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Pope, Shaun Keith. "Control of renal function by peptide hormones in the rainbow trout, Oncorynchus mykiss." Thesis, University of Exeter, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288699.
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Branco, Regiane Cardoso Castelo. "Efeito da angiotensina-(1-7) no fluxo reabsortivo de bicarbonato (JHCO3-) e na concentração citosólica de cálcio ([Ca2+]i): estudo por microperfusão tubular proximal, in vivo." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-25072012-135726/.
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O estudo avaliou os efeitos agudos da Ang-(1-7) na reabsorção de bicarbonato (JHCO3-) no túbulo proximal cortical de rato, in vivo, medindo o pH intratubular pelo microeletródio sensível a H+. O JHCO3- controle é 2,84 ± 0,08 nmol. cm-2. s-1 (49), a Ang-(1-7; 10-12 ou 10-9 M) o reduz (35 ou 61 %) e a Ang-(1-7; 10-6 M) o eleva (56 %). A inibição do receptor Mas (por A779) eleva o JHCO3- (30 %), abole o efeito inibidor da Ang-(1-7), mas não afeta seu efeito estimulador. A inibição do NHE3 (por S3226) diminui o JHCO3- (45 %), não altera o efeito inibidor da Ang-(1-7), mas transforma seu efeito estimulador em inibidor. A concentração de cálcio citosólico ([Ca2+]i), medida pelo FURA-2-AM, controle é 100 ± 2,47 nM (35) e a Ang-(1-7; 10-12, 10-9 ou 10-6 M) a aumenta (152, 103 ou 53 %) transientemente (3 min). A inibição do receptor Mas aumenta a [Ca2+]i (26 %), mais inibe o efeito estimulador de todas as doses de Ang-(1-7). Os resultados indicam que o efeito bifásico dose-dependente da Ang-(1-7) sobre o JHCO3- no túbulo proximal é via receptor Mas e isoforma NHE3 e sugerem estimulação desse trocador por moderado aumento da [Ca2+]i na presença de Ang-(1-7; 10-6 M) e sua inibição por pronunciado aumento da [Ca2+]i na vigência de Ang-(1-7; 10-12 ou 10-9 M).The action of Ang-(1-7) on bicarbonate reabsorption (JHCO3-) was evaluated in vivo middle proximal tubule of rat kidney, using H ion-sensitive microelectrodes. The control JHCO3- is 2,84 ± 0.08 nmol. cm-2. s-1 (49), Ang-(1-7; 10-12 or 10-9 M) decreases it (35 and 61 %) but Ang-(1-7; 10-6 M) increased it (56 %). A779 (an Ang-(1-7) receptor Mas antagonist) increases the JHCO3- (30 %), prevents the inhibitory effect of Ang-(1-7) and does not affect the stimulatory effect of Ang-(1-7). S3226 (10-6 M; an inhibitor of NHE3) decreases the JHCO3- (45 %), does not affect the inhibitory effect of Ang-(1-7) and changes its stimulatory effect on an inhibitory effect. The control cytosolic free calcium ([Ca2+]i), monitored by FURA-2-AM, is 100 ± 2,47 nM (35) and Ang-(1-7; 10-12, 10-9 or 10-6 M) causes a transient (3 min) increase of it (152, 103 or 53 %). A779 increases the [Ca2+]i (26 %) but impaired the stimulatory effect of Ang-(1-7). Our results indicate the biphasic dose-dependent effect of Ang-(1-7) on JHCO3- in proximal tubule is mediated via Mas receptor and NHE3 and are compatible with stimulation of this exchanger by a moderate increase in [Ca2+]i in the presence of Ang-(1-7, 10-6 M), and its inhibition by large increase in [Ca2+]i with Ang-(1-7, 10-12 or 10-9 M).
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Diniz, Gabriela Placoná. "Avaliação da contribuição do receptor AT1 de angiotensina II e do papel da via de sinalização AKT/GSK-3/mTOR no processo de hipertrofia do cardiomiócito induzido pelo hormônio tiroideano." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-25032010-143422/.
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O presente estudo avaliou o papel do receptor AT1 de Angiotensina II no desenvolvimento da hipertrofia dos cardiomiócitos promovida pelo T3, bem como a participação dos mecanismos intracelulares deflagrados pelo receptor AT1 neste modelo de hipertrofia cardíaca. O silenciamento do receptor AT1 com RNA de interferência preveniu totalmente o desenvolvimento da hipertrofia dos cardiomiócitos induzida pelo T3. Os cardiomiócitos tratados com T3 demonstraram uma rápida ativação da via da Akt/GSK-3/mTOR, a qual foi atenuada ou prevenida pelo silenciamento do receptor AT1. Ainda, a expressão de Angiotensina I/II no lisado celular e a expressão do receptor AT1 foram rapidamente aumentados pelo T3. Esses dados demonstram pela primeira vez que o receptor AT1 é um mediador crítico da hipertrofia dos cardiomiócitos induzida pelo T3, bem como para a ativação da via da Akt, sugerindo que a via Ang I/II-AT1-Akt/GSK-3/mTOR corresponde a um potencial mediador dos efeitos tróficos exercidos pelo T3 nessas células.The present study investigated the role of Angiotensin type 1 receptor (AT1R) in T3-induced cardiomyocyte hypertrophy, as well as the participation of the intracellular mechanisms mediated by AT1R in this cardiac hypertrophy model. The AT1R silencing using small interfering RNA totally prevented the development of T3-induced cardiomyocyte hypertrophy. The cardiomyocytes treated with T3 demonstrated a rapid activation of Akt/GSK-3/mTOR signaling pathway, which was attenuated or prevented by the AT1R silencing. In addition, local Angiotensin I/II (Ang I/II) levels and the AT1R expression were rapidly increased by T3 treatment. These data demonstrate for the first time that the AT1R is a critical mediator to the T3-induced cardiomyocyte hypertrophy, as well as to the activation of the Akt signaling, suggesting that the Ang I/II-AT1R-Akt/GSK-3/mTOR pathway corresponds to a potential mediator of the trophic effect exerted by T3 in cardiomyocytes.
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McNeill, Helen. "Angiotensin II and MAP kinase in the rat adrenal gland." Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268825.
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Rigby, M. "The neuromodulatory actions of angiotensin II." Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374445.
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Costa, Rafaela 1984. "Ação modulatória da estimulação tátil e do enriquecimento ambiental sobre as respostas hormonais e comportamentais induzidas por estresse crônico, em ratos." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314212.
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Orientador: Fernanda Klein MarcondesTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Dados da Organização Mundial de Saúde mostram que atualmente a depressão atinge 121 milhões de pessoas e deverá ser a doença mais comum no mundo em 2020. Evidências científicas mostram sua associação com o estresse crônico e alterações neuronais relacionadas à depressão, ansiedade, prejuízo no aprendizado e memória. A qualidade do ambiente em que o indivíduo está inserido e o suporte social de que dispõe representam os principais fatores na regulação dessas alterações. Com relação aos mecanismos fisiopatológicos envolvidos nos efeitos do estresse crônico, há estudos que demonstram uma importante associação entre estresse e hiperatividade do sistema renina angiotensina (SRA). Porém, os mecanismos envolvidos na associação entre estresse e depressão e nos efeitos protetores de condições ambientais favoráveis ainda não estão esclarecidos. Em modelo animal, a intervenção ambiental por meio da estimulação tátil ou enriquecimento ambiental tem sido proposta como um fator que poderia diminuir o estresse e promover o bem-estar. No experimento 1, o objetivo deste estudo foi avaliar os efeitos da intervenção ambiental, por meio da estimulação tátil (manipulação) ou enriquecimento ambiental, sobre as respostas hormonais e comportamentais induzidas pelo estresse crônico moderado e imprevisível (ECMI) em ratos Sprague-Dawley jovens. Nesse estudo foi evidenciado que o ECMI aumentou as concentrações séricas de corticosterona e plasmáticas de noradrenalina e adrenalina; induziu comportamentos análogos à depressão; prejudicou o aprendizado e memória e aumentou a concentração tecidual de angiotensina I, II e IV no hipotálamo. Tanto a manipulação quanto o enriquecimento ambiental atenuaram a secreção hormonal, os comportamentos análogos à depressão e o aumento de angiotensina II no hipotálamo; e cancelaram o prejuízo cognitivo induzido pelo ECMI. Com o objetivo de estudar se os efeitos da angiotensina II, mediados pelo receptor tipo 1 de angiotensina II (AT1), estão envolvidos nas respostas hormonais e no prejuízo cognitivo induzido pelo ECMI, no experimento 2, ratos machos Sprague-Dawley controles e estressados, tratados ou não com losartan (antagonista de receptor AT1) foram avaliados. Nesse experimento, a administração do losartan cancelou o aumento na secreção dos hormônios do estresse, atenuou o desamparo aprendido e o prejuízo cognitivo em animais estressados. Os resultados obtidos mostraram que a manipulação ou o enriquecimento ambiental produzem efeitos hormonais e comportamentais positivos capazes de melhorar o bem-estar animal e podem diminuir os efeitos deletérios induzidos por estresse crônico em ratos jovens. Além disso, sugerem que a atividade do sistema renina-angiotensina pode estar envolvida nos efeitos negativos desencadeados pelo estresse crônico
Abstract: Data from the World Health Organization show that depression currently affects 121 million people and will probably be the most common disease in the world in 2020. Scientific evidences show that it is associated with chronic stress, neuronal changes depression-related, anxiety and impairment in learning and memory. There are also a significant association between stress and hyperactivity of the renin angiotensin system on behavioral changes and cardiovascular effects. It is also noteworthy that the quality of the environment in which the individual belongs and the social support represent the main factors that may regulated these effects. In addition, the pathophysiological mechanisms involved in the association between stress and depression, and the protective effects of favorable environmental conditions remain unclear. In animal models, environmental intervention through tactile stimulation (handling) or environmental enrichment have been proposed as factors that may reduce stress and promote well-being. In the experiment 1, the objective of this study was to evaluate the effects of environmental intervention, through tactile stimulation (handling) or environmental enrichment on behavioral and hormonal responses induced by chronic mild unpredictable stress (CMS) in young Sprague-Dawley rats. The results of this study showed that the CMS increased serum corticosterone, plasma norepinephrine and epinephrine concentrations; induced depression-like behaviors; impaired learning and memory and increased hypothalamus angiotensin I, II and IV. Handling and environmental enrichment attenuated stress hormones secretion, depression-like behaviors and increased hypothalamic angiotensin II levels; and cancelled impairment of learning and memory induced by CMS. Considering that the aim of study 1 was evaluate if the effects of angiotensin II, mediated by angiotensin II type 1 receptor (AT1), are involved in hormone responses and cognitive impairment induced by CMS, the experiment 2 were performed. In the second study, male Sprague-Dawley rats controls and stressed, treated or not with losartan (AT1 receptor antagonist) were evaluated. Results from the second study showed that the losartan administration cancelled the increase in stress hormones secretion, attenuated depression-like behaviors and reduced the impairment of learning and memory in stressed animals. The data obtained indicated that the handling or environmental enrichment produced positive hormonal and behavioral effects capable of improving the animal¿s welfare, diminishing the deleterious effects induced by chronic stress in adult rats. The results also suggest that renin-angiotensin system over activity seems to be involved in negative effects of CMS
Doutorado
Fisiologia
Doutora em Biologia Funcional e Molecular
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Lee, Alison Frances Clare. "The renin angiotensin aldosterone axis : relationships with other hormone systems, and novel applications for angiotensin converting enzyme inhibitors." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/22401.
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The aim of this thesis was to look at the renin angiotensin system both in clinical heart failure, and in relation to other physiological systems where an interaction may exist. Furthermore, to address new areas where a potential for benefit with Angiotensin Converting Enzyme (ACE) inhibitors might occur. To this end there are five studies discussed within the thesis. It is shown that in a group of heart failure patients, stabilised on maximum tolerated dose of ACE inhibitor, mean levels of plasma neurohormones were remarkably stable over 18 months. Reactivation of aldosterone occurred in 13/97 samples (13.5%) in 5/22 (23%) individuals, and reactivation of angiotensin II occurred in 8/102 samples (8%), in 6/22 (27%) individuals. These appear to be sporadic phenomenon, and contrary to previous dogma, they do not herald disease progression. Using endothelial function as a surrogate marker for cardiovascular events in hyperlipidaemic patients, it is shown that interruption of the renin angiotensin system using ACE inhibition, causes increases in both endothelial dependent and endothelial independent vasodilation. This could lead to the use of ACE inhibitors in hyperlipidaemic patients to reduce cardiovascular events, over and above traditional therapy such as statins. Subsequent to the above, the effect of lisinopril on nitrate/nitrite excretion as a marker of nitric oxide metabolism in hypercholesterolaemia was assessed. The levels of plasma nitrate/nitrite after an eighteen hour fast in twenty of the hyperlipidaemic volunteers were taken, and contrasted with values in normal volunteers. Lisinopril was found to have no effect on nitrate/nitrite levels in the hyperlipidaemic patients. Evidence in the literature has suggested interactions between the renin angiotensin system, and oestradiol, whose mechanism of vasodilation is still under debate. This study, using forearm plethysmography, looked at whether vasodilation by ovarian hormones was due to effects on the renin angiotensin system. No evidence was found that either oestradiol, or medroxy-progesterone affected vascular responses to angiotensin II, or altered the activity of vascular ACE activity.
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Tavares, Felix Meira. "Efeito do hormônio tiroideano na função cardíaca no modelo de isquemia/reperfusão em ratos. Papel do receptor AT2 e da via intracelular AMPK." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-24072012-131445/.
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Os Hormônios Tiroideanos (HT) representam um fenótipo de cardioproteção e influenciam no estado trófico do tecido cardíaco através de diversos mecanismos, dentre eles a modulação dos componentes do Sistema Renina Angiotensina- a Angiotensina II e seus receptores (AT1 e AT2). Este estudo teve como objetivos avaliar o papel do receptor AT2 na cardioproteção induzida pelo HT e a participação da proteína quinase ativada por AMP (AMPK) nesse processo. O modelo de isquemia e reperfusão (I/R) foi desenvolvido em corações de ratos submetidos ao hipertiroidismo experimental na presença ou ausêcia do antagonista do receptor AT2 (PD123319), utilizando-se o aparto de Langendorff. Os resultados mostraram que o HT exerce efeito cardioprotetor com aumento na expressão protéica do receptor AT2 e da AMPK fosforilada, que foi prevenido com a administração do PD, seguido de piora da função cardíaca. Estes dados sugerem que parte da cardioproteção induzida pelo HT é mediada pelo receptor AT2, e que a AMPK também está envolvida proteção do miocárdio após injúria por I/R.Thyroid Hormones (TH) is a phenotype of cardioprotection and may influence the trophic state of cardiac tissue through several mechanisms, including the modulation of the components of renin-angiotensin system - angiotensin II and its receptors (AT1 and AT2). The present study aimed to evaluate the role of AT2 receptor in cardioprotection mediated by the TH and the involvement of AMP-activated protein kinase (AMPK) in this context. A model of Ischemia and Reperfusion (I/R) was performed in isolated hearts of rats subjected to experimental hyperthyroidism, in the presence or absence of the AT2 receptor antagonist (PD123319), using the Langendorff system. The results showed that TH exerts cardioprotective effect with increased levels of AT2 and phosphorylated AMP protein expression, which was prevented by the administration of PD, with a loss in cardiac function. These data suggest that part of the TH-induced cardioprotection is mediated by the AT2 receptor with the involvement of AMPK in protection of the myocardium after I/R injury.
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Schmid, Ursula. "Protection against oxidative DNA damage by antioxidants, hormone-receptor blockers and HMG-CoA-reductase inhibitors." Doctoral thesis, kostenfrei, 2008. http://nbn-resolving.de/urn/resolver.pl?urn=nbn:de:bvb:20-.
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Mielke, Marilyn. "Mechanisms underlying the inotropic response to angiotensin II in the heart." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325976.
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David, Richard Boarato. "Especificidade do apetite ao sódio: uma possível contribuição hormonal." Universidade Federal de São Carlos, 2006. https://repositorio.ufscar.br/handle/ufscar/1282.
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Previous issue date: 2006-08-24The hypothesis of a synergy between two hormones responsible for sodium conservation, aldosterone and angiotensin II (ANG II), explains the expression of a characteristic of sodium appetite, hypertonic NaCl intake, in a hypovolemic animal. Hypertonic NaCl intake can be induced in normovolemic rats that received a combined treatment of mineralocorticoid and ANG II at individual doses not sufficient to induce sodium intake (paradigmatic synergy test). Considering the motivation to specific sodium intake another characteristic of sodium appetite, the objective of the present dissertation was to find out a role for the interaction between mineralocorticoid and ANG II on the specificity of sodium appetite. Sprague-Dawley Holtzman rats (≅ 300 g b.w.) were housed with access to water and one or more palatable (0.01 M KCl, 0.05 mM CaCl2, 0.15 M NaHCO3, 0.15 M NaCl) or hypertonic (0.50 M NaCl) mineral solutions for ingestion. In two-bottle tests, a bottle contained water and another bottle contained either 0.01 M KCl, 0.15 M NaHCO3, 0.15 M NaCl or 0.50 M NaCl. In five-bottle tests, a bottle contained water and each one of the remaining four bottles contained either 0.01 M KCl, 0.05 mM CaCl2, 0.15 M NaHCO3 or 0.15 M NaCl, respectively. In sodium depletion tests, intact rats received each a 10 mg sc. injection of furosemide or vehicle followed by 24 h access to sodium deficient food and water. Then, food was removed and mineral solutions and water were offered for recording their intake (sodium appetite test). In the paradigmatic synergy test, the animals received daily single sc injection of 2.5 mg of deoxycorticosterone acetate (DOCA) or sunflower oil (vehicle) for three days and a left lateral cerebroventricular injection of 50 ng of ANG II four hours after the last DOCA or oil injection. Fluid intake record began immediately after ANG II injection and food removal. The daily intake record showed no preference for any solution or water when animals had access to five bottles. Sodium depletion induced a preferential sodium intake, with higher NaCl than NaHCO3 intake, in either two- or five-bottle sodium appetite tests. DOCA alone enhanced the daily 0.15 M NaCl and NaHCO3 intake, but did not alter KCl or 0.50 M NaCl intake in two-bottle tests. In the paradigmatic tests with normovolemic animals, ANG II combined to oil induced the ingestion of all three palatable mineral solutions (KCl, NaHCO3, NaCl) and water, in two-bottle tests, and preference for NaHCO3 in five-bottle tests. DOCA pretreatment enhanced only sodium solution intake, particularly NaCl intake, induced by ANG II in two-bottle tests (0.15 M NaCl: DOCA/ANG II = 24.5 ± 6.7 ml/120 min. vs. OIL/ANG II = 9.2 ± 1.8 ml/120 min.; 0.15 M NaHCO3: DOCA/ANG II = 17.0 ± 1.8 ml/120 min. vs. OIL/ANG II = 14.6 ± 2.1 ml/120 min.; 0.01 M KCl: DOCA/ANG II = 9.8 ± 1.9 ml/120 min. vs. 11.9 ± 1.2 ml/120 min.), and enhanced by 80 % the total sodium solution intake in the beginning of the five-bottle test. The combined effect of DOCA with ANG II on the induction of 0.50 M NaCl intake in a two-bottle test was replicated in our animals. The results from the paradigmatic synergy test are coherent with results from sodium appetite tests, suggesting that the mineralocorticoid may turn the effect of ANG II on mineral intake more selective to sodium intake. Thus, the combined ANG II and mineralocorticoid action could contribute to the expression of two characteristics of sodium appetite, not only the acceptance of hypertonic sodium solutions, but also the selective sodium intake.
A hipótese do sinergismo entre dois hormônios responsáveis pela conservação de sódio, a aldosterona e a ANG II, explica uma característica do apetite ao sódio, a ingestão de NaCl hipertônico em um animal hipovolêmico. Ingestão de NaCl hipertônico pode ser induzida em ratos normovolêmicos que receberam um tratamento combinado de mineralocorticóide e ANG II, em doses individuais insuficientes para induzir a ingestão de sódio (teste paradigmático do sinergismo). Sendo a motivação para uma ingestão específica de sódio uma outra característica do apetite ao sódio, o objetivo desta dissertação foi o de procurar um papel para a interação entre mineralocorticóide e ANG II na especificidade do apetite ao sódio. Foram utilizados ratos Sprague-Dawley Holtzman (≅ 300 g p.c.) ambientados com livre acesso a bebedouros com água e uma ou mais soluções minerais palatáveis (KCl 0,01 M, CaCl2 0,05 mM, NaHCO3 0,15 M, NaCl 0,15 M) ou hipertônica (NaCl 0,50 M). Em testes de dois bebedouros, um dos bebedouros continha água e o outro, solução de KCl 0,01 M, NaHCO3 0,15 M, NaCl 0,15 M ou NaCl 0,50 M. Em testes de cinco bebedouros, um dos bebedouros continha água e cada um dos demais uma solução de KCl 0,01 M, CaCl2 0,05 mM, NaHCO3 0,15 M ou NaCl 0,15 M. Testes com dois ou cinco bebedouros foram empregados em animais depletados de sódio e no teste paradigmático do sinergismo. Nos testes de depleção de sódio, os animais receberam injeção sc de 10 mg de furosemida ou veículo, seguida de acesso a uma dieta hipossódica e água por vinte e quatro horas. Em seguida, o alimento foi removido e foram oferecidas soluções minerais para registro da ingestão das mesmas e de água (teste do apetite ao sódio). No teste paradigmático do sinergismo, os animais receberam injeção sc de 2,5 mg de acetato de desoxicorticosterona (DOCA) ou óleo de girassol (veículo) uma vez ao dia, durante três dias, e uma injeção de 50 ng de ANG II (ou salina) no ventrículo lateral esquerdo, quatro horas após a última injeção de DOCA ou óleo. Passou-se a registrar a ingestão de líquidos imediatamente após a injeção de ANG II e remoção da ração. O registro da ingestão diária mostrou que não houve preferência por nenhuma solução ou água durante o período de ambientação com cinco bebedouros. A depleção de sódio induziu ingestão preferencial de sódio no teste do apetite ao sódio, sendo a ingestão de NaCl 0,15 M maior do que a de NaHCO3 tanto nos testes de dois como de cinco bebedouros. O tratamento com apenas DOCA aumentou a ingestão diária de NaCl 0,15 M e de NaHCO3 sem alterar a ingestão diária de KCl e de NaCl 0,50 M, em testes de dois bebedouros. No teste paradigmático com ratos normovolêmicos, a ANG II combinada ao óleo promoveu ingestão das três soluções minerais palatáveis (KCl, NaHCO3, NaCl) e de água em testes de dupla escolha, e preferência ao NaHCO3 no teste com cinco bebedouros. O pré-tratamento com DOCA potenciou o efeito da ANG II apenas sobre a ingestão das soluções sódicas, mais evidente para NaCl, no teste com dois bebedouros (NaCl 0,15 M: DOCA/ANG II = 24,5 ± 6,7 ml/120 min. vs. ÓLEO/ANG II = 9,2 ± 1,8 ml/120 min.; NaHCO3 0,15 M: DOCA/ANG II = 17,0 ± 1,8 ml/120 min. vs. ÓLEO/ANG II = 14,6 ± 2,1 ml/120 min.; KCl 0,01 M: DOCA/ANG II = 9,8 ± 1,9 ml/120 min. vs. 11,9 ± 1,2 ml/120 min.), além de aumentar em 80 % a ingestão total de soluções sódicas no início do teste com cinco bebedouros. O efeito da indução de ingestão de NaCl 0,50 M pela combinação de DOCA com ANG II em testes de dois bebedouros foi replicado nos nossos animais. Os resultados do teste paradigmático do sinergismo são coerentes com os testes do apetite ao sódio, sugerindo que o mineralocorticóide possa tornar mais seletivo o efeito da ANG II sobre a ingestão mineral. Assim, uma interação entre ANG II e mineralocorticóide poderia contribuir para a expressão de duas características do apetite ao sódio, não apenas a aceitação de soluções hipertônicas de NaCl, mas também a ingestão seletiva de sódio.
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Goldstein, Bradley E. "Thirst and sodium appetite in mice angiotensin, brain Fos, blood plasma hormones, and fluid intake /." [Gainesville, Fla.] : University of Florida, 2003. http://purl.fcla.edu/fcla/etd/UFE0000687.
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Couraud, Pierre-Olivier. "Anticorps antiidiotypiques diriges contre le recepteur beta-adrenergique et le recepteur de l'angiotensine ii." Paris 7, 1987. http://www.theses.fr/1987PA077027.
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Viard, Isabelle. "Régulation par les hormones et les facteurs de croissance des fonctions spécifiques des cellules surrénaliennes." Lyon 1, 1991. http://www.theses.fr/1991LYO1T208.
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Tabrizchi, Reza. "Different modes of vasopressor actions of angiotensin and non-selective or selective beta-adrenoceptor antagonists." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29439.
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Vasoconstriction can be initiated via the interaction of a number of chemicals with specific "receptive sites" known as the receptors. This thesis examines two distinctly different modes by which drugs initiate a contractile response, namely, (i) the interaction of angiotensin analogues with a heterogeneous population of angiotensin receptors in vascular smooth muscles, and (ii) the conditions whereby B-adrenoceptor antagonists interact with a-adrenoceptor antagonists thereby causing a pressor response. Conscious,
unrestrained, instrumented-rats were used for the study.
It has been suggested that angiotensin receptors in vascular and non-vascular tissues may not be of a homogeneous population. The first study examined whether a heterogeneous population of angiotensin receptors was responsible for increasing vascular tone. Dose-response curves were constructed for angiotensin II (ANG II) and des Asp¹ angiotensin II (ANG III) on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of total body venous tone, in the presence or absence of [Sar¹, Ile⁸]ANG II. The i.v. infusion of ANG II or ANG III caused dose-dependent increases in MAP and MCFP. In the presence of [Sar¹, Ile⁸]ANG II, the MAP and MCFP curves for ANG II were displaced to the right with pA₂ values of 9.2 and 8.4 for the arterioles and veins, respectively. However, the antagonist displaced dose-MCFP but not the dose-MAP response curve of ANG III. This suggests that ANG II and ANG III act on the same receptor in veins but not arterioles. This concept was further investigated by obtaining dose-MAP and dose-MCFP response curves for ANG II in the presence of ANG II or ANG III. Dose-MAP response curve to ANG II was displaced to the right in the presence of ANG II but not ANG III. Dose-MCFP response curve for ANG II was displaced to the right in the presence of ANG III but not ANG II. These results again suggest that ANG
III acts on the same receptors as ANG II in the veins but not arterioles. In the last series of experiments two analogues of angiotensin III were compared as antagonists of the pressor response to ANG II and ANG III. In the presence of [Ile⁷]ANG III, the dose-MAP response curves for ANG II and ANG III were displaced to the right while in the presence of [Sar¹, Ile⁷]ANG III, the dose-MAP response curve for ANG III but not ANG II was displaced. This suggests that [Sar¹, Ile⁷]ANG III is a selective antagonist of ANG III in the arterioles.
In summary, the results indicate that ANG III acts on a different sub-class of angiotensin receptors than ANG II in the arterioles but it may act as a partial agonist on the same type of receptors as ANG II in the venous bed. Thus, ANG II receptors in the arterioles appear to be different from those in veins.
The administration of a non-selective β-antagonist propranolol into animals subjected to non-selective α-blockade has been observed to cause a paradoxical pressor response. This second study examines whether the paradoxical
pressor response to β-antagonists was due to: (i) an interaction of a β-antagonist with an α-antagonist, (ii) blockade of vasodilator β₂-adrenoceptors or (iii) an increase in the release of catecholamines. Cumulative dose-response curves for propranolol, atenolol (β₁-antagonist) and ICI 118,551 (β₂-antagonist) were obtained in rats subjected to a continuous i.v. infusion of phentolamine, a non-selective α-antagonist. The administration of each of the β-antagonists caused a dose-dependent increase in MAP suggesting that the pressor response was not due to the blockade of vasodilator β₂-adrenoceptors. Another four groups of phentolamine-treated rats were given a single i.v. bolus injection of saline, propranolol, atenolol or ICI 118,551, and sampling of arterial blood for the determination of adrenaline (A) and noradrenaline (NA) concentration by HPLC/ec. Phentolamine caused a decrease in MAP and an increase in the plasma levels of A and NA. Subsequent injection of propranolol, atenolol and ICI 118,551 but not saline increased MAP. Neither saline nor any of the β-antagonists increased plasma NA or A levels suggesting that the pressor response was not associated with an acute increase in the release of catecholamines. It was also shown that prior injection of a β-antagonist partially antagonized the hypotensive effect of phentolamine suggesting that the pressor response was related to an interaction between α- and β-antagonists.
It was further shown that a continuous infusion of either prazosin or rauwolseine caused a small but not significant decrease in MAP which was reversed by propranolol. Concurrent infusions of prazosin and rauwolscine caused a large decrease in MAP. Subsequent injection of propranolol caused a large pressor response. On the contrary, sodium nitroprusside or metha-choline each decreased MAP but the hypotension was not antagonized by propranolol. These results were consistent with the existence of a specific interaction between α- and β-antagonists.
These experiments demonstrated that although the mechanisms involved in the initiation of a change in vascular tone did not share a common pathway,
the final outcome shared a common denomination.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Boyer, Hadrien. "Contribution à l'étude de l'influence du système immunitaire sur la sécrétion des hormones corticosurrénaliennes." Rouen, 2015. http://www.theses.fr/2015ROUES014.
Full textAbstract:
Le cortex surrénalien est infiltré par des cellules du système immunitaire, dont les mastocytes, et exprime de nombreux récepteurs pour divers facteurs, tels que les récepteurs de l’ACTH mais aussi ceux des cytokines impliquées dans la réponse de l’organisme à une infection systémique. Cette interaction entre la fonction corticosurrénalienne et le système immunitaire jouerait un rôle important dans la réponse de l’organisme au stress infectieux en contribuant à maintenir l’homéostasie hydrominérale et métabolique. Des données antérieures ont montré que les mastocytes intrasurrénaliens stimulent la production d’aldostérone chez l’homme et le rat mais le rôle des cellules mastocytaires dans la régulation de la production de minéralocorticoïdes reste imprécis. Nos résultats montrent que les souris déficientes en mastocyte KitW-sh/W-sh présentent en régime normosodé une activation du système rénine-angiotensine (SRA) circulant qui permet de maintenir des taux normaux d’aldostérone plasmatique. En régime hyposodé, l’absence de mastocyte s’associe à une forte stimulation de l’expression de la rénine intra-surrénalienne à l’origine d’un hyperaldostéronisme majeur. Ces deux phénomènes peuvent être considérés comme des mécanismes de compensation consécutifs au déficit en mastocyte et suggèrent ainsi un rôle physiologique des mastocytes surrénaliens dans la régulation de la synthèse et de la production d’aldostérone. D’autres observations viennent conforter cette hypothèse comme l’activation des mastocytes surrénaliens par le régime désodé ainsi que la réduction de l’activité mastocytaire aux niveaux rénal et surrénalien en réponse au traitement par l’aliskiren, inhibiteur de la rénine circulante, chez les souris sauvages. Au cours du sepsis, la réponse sécrétoire de la surrénale dépend de la montée de l’ACTH et des cytokines à laquelle se surajoute l’influence du lipopolysaccharide (LPS). La synthèse intense de glucocorticoïdes en réponse au stress nécessite un apport important en cholestérol dans les cellules corticosurrénaliennes. Un défaut en protéines impliquées dans la stéroïdogenèse peut être responsable de la production inadaptée de cortisol observée chez les patients en choc septique. Grâce à l’utilisation d’un modèle murin de sepsis par ligature caecale, nous montrons que le sepsis augmente l’expression du gène codant SR-B1, le récepteur du HDL-cholestérol, mais réduit celle des gènes du transporteur Star et des enzymes de la stéroïdogenèse 3βHSD et 21-hydroxylase. Le traitement prolongé de souris et de cellules corticosurrénaliennes de rat par du LPS entraine une réduction progressive de la synthèse de corticostérone en réponse à l’ACTH. De plus, l’immunoréactivité des protéines SR-B1 et 3βHSD est fortement réduite dans le cortex surrénalien des souris traitées au LPS ainsi que dans celui des patients décédés de choc septique. Ces résultats montrent que la diminution de l’expression des gènes codant les transporteurs du cholestérol et les enzymes de la stéroïdogenèse joue un rôle important dans le développement d’une insuffisance surrénalienne lors d’un sepsis.
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Prosser, Hamish Charles Graydon. "Involvement of Novel Cardiac Peptides in Healthy and Ischemic Hearts." Thesis, University of Canterbury. Biological Sciences, 2009. http://hdl.handle.net/10092/2731.
Full textAbstract:
The role and functions of Urotensin II (UII), Urotensin II-related peptide (URP) and proangiotensin-12 (PA12) are currently ambiguous, either due their relatively new identification and isolation from their host species, or due to contrasting and conflicting reports observing the physiological and pathophysiological role of these spasmogens within the mammalian cardiovascular system. Accordingly, we sought to determine the true physiological functions of these peptides in both healthy and diseased states. The initial task was to reveal potential reasons for the contrasting responses to UII, and to define the role of UII within the isolated rat heart. UII and URP retain a highly conserved cyclic region, shown to be necessary in receptor binding and activation, with the high inter-species variance within the N-terminus reported to be of little importance. Our research revealed UII to be highly species-specific, stimulating potent, sustained vasodilation of the coronary arteries in response to the native form infused, while non-native UII peptides had either no effect, or caused significant vasoconstriction. UII-induced vasodilative effects were found to be mediated by nitric oxide and prostaglandin activity combined. Reviewing publications to date it was evident that many studies employed UII foreign to the host species, reporting potentially untrue effects, based on our findings. Recent studies have identified UII as a potent agent in developing and promoting atherosclerosis and coronary artery disease through UII-induced mitogenic activity and promoting foam cell formation. Hence, we observed the effect of infusing the native species of UII and URP into a model of cardiac ischemia-reperfusion. Both preconditioning the heart with UII or URP, or infusing UII or URP upon reperfusion caused significant coronary vasodilation following ischemia, and significantly attenuated ischemic-induced myocardial injury. These studies indicated elevating UII and URP provided a level of cardioprotection, not only when administered into healthy hearts prior to an ischemic event, but also in hearts having already undergone ischemia and the resultant endothelial damage. PA12 was the third peptide tested in the current thesis. Being newly identified and suggested to be a new component of the renin-angiotensin system (RAS) it was important to define the physiological role of PA12 upon the cardiovasculature, as the RAS is heavily associated with the development and progression of cardiovascular disease. Utilising the Langendorff isolated rat heart technique, PA12 was found to cause potent vasoconstriction of the coronary arteries, mediated by the angiotensin II type 1 receptor (AT₁R). Furthermore, using subjecting the perfusate samples to radioimmunoassay and RP-HPLC revealed PA12 was converted to AngII. Both PA12-induced vasoconstriction and generation of AngII were found to be dependent upon chymase activity, with inhibition of ACE1 having little effect. Myography was employed to further study the vascular response to PA12 throughout the rat arterial system from the common carotid to the femoral arteries. PA12-induced vasoconstriction displayed a potency gradient, with greatest constriction observed in vessels closest to the heart, with potency reduced and eventually lost further from the heart. PA12-induced vasoactivity was shown to be dependent upon both chymase and ACE1 activity, with ACE1 regulating PA12 activity with greater potency. The intracellular pathways stimulated in response to PA12 were defined using western blotting, with PA12 stimulating phosphorylation of ERK1/2, JNK, p38 and PKCα/β₁₁, but having no influence on PKCδ/θ. Stimulation of these pathways is consistent with the observed PA12-induced vasoconstriction, and also indicates that PA12 activation of AT₁R and the subsequent cytokines, could potentially stimulate hypertrophy, apoptosis, cell growth and differentiation, and inflammation, promoting cadiovascular remodelling and progressing atherosclerosis, hypertension and other vascular diseases if not sufficiently regulated. Taken together, these studies indicate PA12 may have a primary role within the local, tissue-based RAS, providing an alternate substrate to angiotensin I, while ACE1 is the primary regulatory enzyme within the circulation. Our findings also display the chymase-dependent PA12/AT₁R pathway as potential novel targets for pharmacological inhibition of RAS activity to ameliorate hypertension and maladaptive vascular remodelling.
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Silva, Taíz Francine Brasil da. "Envolvimento da neurotransmissão angiotensinérgica do córtex pré-límbico na modulação de respostas autonômicas, hormonal e status oxidativo evocados pelo estresse de restrição em ratos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-05012017-113115/.
Full textAbstract:
O córtex pré-límbico (PL) é uma importante área límbica envolvida em vários processos funcionais correlatos ao estresse, tais como respostas cardiovasculares, hormonais e comportamentais. O modelo de estresse de restrição (ER) foi padronizado na literatura como uma situação aversiva capaz de promover aumento da pressão arterial e frequência cardíaca, queda da temperatura cutânea e estimulação do eixo hipotálamo-pituitária-adrenal (HPA). Trabalhos da literatura evidenciaram que ratos submetidos ao ER apresentavam aumento da atividade neuronial no PL, sugerindo que essa estrutura module respostas ao ER. Assim, a inibição temporária de sinapses no PL potencializou a resposta taquicárdica induzida pelo ER, sem alterar a resposta pressora. Além do controle cardiovascular, outros trabalhos demonstraram que o PL também participa do controle hormonal durante o ER. O ER agudo também está envolvido com a produção de espécies reativas de oxigênio (EROs), fator que pode estar envolvido nas alterações a longo prazo observadas após exposição a uma situação aversiva. O sistema renina angiotensina (SRA) central modula respostas cardiovasculares, inclusive aquelas induzidas por situações aversivas, além de ter um papel reconhecido na produção de EROs. Além disso, foi demonstrado que o PL possui SRA funcional com presença dos peptídeos a ele relacionados. Baseado nos fatos mencionados acima, a hipótese do presente projeto é que a neurotransmissão angiotensinérgica do PL está envolvida na modulação de respostas autonômicas (aumento de pressão arterial e frequência cardíaca, e queda da temperatura cutânea) e hormonal (aumento plasmático de corticosterona) evocadas pelo ER, e que essa via envolveria a formação de EROs. A microinjeção do inibidor da enzima conversora de angiotensina (ECA) lisinopril no PL, nas doses de 0,5 e 1nmol/100nL, reduziu a resposta pressora, sendo a dose de 1nmol/100nL de lisinopril também capaz de reduzir a resposta taquicárdica induzida pelo ER; porém nenhuma dose utilizada ocasionou mudanças na queda da temperatura cutânea evocada pelo ER. O pré-tratamento do PL com o antagonista de receptores do subtipo AT1 candesartan reduziu o efeito pressor induzido pelo ER, porém não alterou a resposta taquicárdica e queda da temperatura cutânea associadas ao ER. Por sua vez, o pré-tratamento com o antagonista de receptores do subtipo AT2, PD123177, reduziu a resposta taquicárdica sem alterar a resposta pressora e a queda da temperatura cutânea evocadas pelo ER. Em adição, o estresse de restrição agudo e os pré-tratamentos realizados não foram capazes de alterar a atividade da enzima NADPH oxidase no PL. Em conclusão, os presentes resultados sugerem a participação do SRA na modulação da resposta cardiovascular ao ER, através da ativação de receptores AT1, e AT2 do PL, afetando respectivamente, o componente vascular e o cardíaco da resposta autonômica causada pelo ER. Além disso, os resultados da atividade da enzima NADPH oxidase no PL sugerem que o ER agudo, os receptores AT1, AT2 e a ECA não modulam o status oxidativo local.The prelimbic cortex is an important limbic structure involved in several stressrelated functional processes, such as cardiovascular, hormonal and behavior responses. Restraint stress (RS) was standardized in literature as an aversive situation able to promote blood pressure and heart rate increases, reduction in tail temperature and stimulation of the hypothalamic-pituitary-adrenal axis (HPA). Previous studies demonstrated that rats submitted to RS exhibited increased neuronal activity in the PL, suggesting that this structure modulates RS-evoked responses. Temporary, synaptic temporary inhibition in the PL markedly increased the RS-evoked tachycardiac response, without affecting the pressor one. Beyond cardiovascular control, other studies demonstrated that PL also participates in hormonal control during RS. Acute RS is also involved in the production of reactive oxygen species (ROS), which could be involved in long- term changes observed after exposure to an aversive situation. The central renin-angiotensin system (RAS) modulates cardiovascular responses, including those induced by aversive situations. In addition, this system has a well-known role in ROS production. Furthermore, the presence of angiotensinergic peptides in PL has also been demonstrated, suggesting the existence of a functional RAS in this structure. Based on the facts mentioned above, the hypothesis of the present study was that the angiotensinergic neurotransmission in PL is involved in the modulation of autonomic responses (blood pressure and heart rate increase, and reduction in tail temperature) evoked by RS, and this pathway would involve ROS formation. Microinjection of lisinopril (0.5 and 1nmol/100nL), an inhibitor of angiotensinconverting enzyme (ACE), into PL reduced the pressor response, and the dose 1nmol/nL was also able to reduce the tachycardiac response induced by RS; however, none of doses changed the reduction in tail temperature evoked by RS. PL treatment with candesartan, an AT1 receptors antagonist, reduced the RS-evoked pressor response, but did not affect the RS-evoked tachycardiac response and reduction in tail temperature. In addition, pretreatment with PD123177, an AT2 receptors antagonist, reduced the RS-evoked tachycardiac response, without affecting the pressor response or the RS-evoked reduction in tail temperature. In addition, neither acute RS or local treatments affected NADPH oxidase activity in the PL. In conclusion, the present results suggests the involvement of the central RAS in the modulation of the cardiovascular responses caused by RS, through the activation of both AT1 and AT2 receptors in the PL. The PL AT1 receptors modulating the vascular, and the AT2 modulating the cardiac component of RS-evoked autonomic response. Furthermore, our study suggests that neither acute RS or local AT1, AT2 and ACE affect oxidative status in the PL.
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Takano, Ana Paula Cremasco. "Fatores relacionados à inflamação na hipertrofia cardíaca induzida pelo hormônio tiroideano. Contribuição do sistema renina-angiotensina." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-09082016-100628/.
Full textAbstract:
O presente estudo avaliou aspectos relacionados ao contexto inflamatório na hipertrofia cardíaca induzida pelos hormônios tiroideanos (HT) e o possível envolvimento do sistema renina-angiotensina (SRA) nesse processo, utilizando análises in vivo e com enfoque maior na abordagem in vitro. Os resultados mostraram algumas alterações em citocinas circulantes e cardíacas de animais tratados com HT. Além disso, as expressões de S100A8 e MyD88 foram aumentadas no coração de ratos submetidos ao hipertiroidismo e em cardiomiócitos em cultura estimulados com HT. S100A8 e MyD88 mediaram a ativação do fator nuclear NF-κB pelos HT, tendo papel crucial para o crescimento hipertrófico de cardiomiócitos tratados com HT. Por fim, a ação dos HT modulando a expressão de S100A8 e NF-κB foi mediada pelo SRA. Estes dados contribuem com o entendimento das bases moleculares da ação dos HT e da relação deste com o SRA na hipertrofia cardíaca.The present study evaluated inflammation related aspects in cardiac hypertrophy induced by thyroid hormones (TH) and the possible involvement of the renin-angiotensin system (RAS) in this process, by using in vivo and in vitro analysis. The results showed alterations in circulating and cardiac cytokines from TH treated animals. The expression of S100A8 and MyD88 were increased in the heart of hyperthyroid rats and in cultured cardiomyocytes stimulated with TH. S100A8 and MyD88 mediated the nuclear factor NF-κB activation by TH and these factors presented crucial role to the hypertrophic growth of TH-treated cardiomyocytes. Finally, the action of TH on S100A8 and NF-κB expression was mediated by RAS. These data contribute to the knowledge of molecular basis of TH action and the relationship between TH and RAS in cardiac hypertrophy.
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Schadock, Ines Claudia. "Physiological role of prolylcarboxypeptidase." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16412.
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Prolylcarboxypeptidase (PRCP, EC3.4.16.2) ist ein ubiquitär exprimiertes Enzym, mit höchster Expression im Maushirn. Es spaltet spezifisch die letzte carboxyterminale Aminosäure von Substraten, deren vorletzte Aminosäure ein Prolin ist. Seine bisher publizierten Substrate Angiotensin II (AngII) und alpha Melanocortin Stimulierendes Hormone (alphaMSH) legen eine Rolle von PRCP in der Entwicklung von kardiovaskulären und metabolischen Krankheiten nahe. Um die in vivo Funktion von PRCP zu studieren, wurde eine Knockout Maus generiert (PRCP-/-). Metabolischer Phänotyp: PRCP-/- Mäuse zeigten generell ein reduziertes Körpergewicht, selbst wenn sie über Monate mit einer Hochfettdiät versorgt wurden. Erhöhte Plasmaleptin Werte und Proopiomelanocortin (pomc) Expression in knockout Hypothalami wiesen auf eine wichtige Rolle von PRCP in der Regulation von Futteraufnahme und Energiehomöostase hin. Eines der Genprodukte von pomc ist alphaMSH, welches im Hypothalamus die Futteraufnahme terminiert. Die carboxyterminale Struktur dieses Neuropeptids erfüllt alle Voraussetzungen, um von PRCP gespalten zu werden. Zudem konnte prcp Promotoraktivität in den selben Hirnstrukturen gezeigt werden, in denen auch alphaMSH-Wirkung beschrieben wurde. Eine mögliche Funktion von PRCP wäre somit die Inaktivierung des Appetitzüglers alphaMSH im Hypothalamus. Kardiovasculärer Phänotyp: Zunächst erwiesen sich zirkulierende Ang-Peptide in PRCP-/- Mäusen als unverändert. Jedoch konnte ein erhöhtes Niveau des Degradationsproduktes Ang1-7 in der Niere gezeigt werden. Die Entdeckung einer erhöhten Enzymaktivität von Angiotensin Converting Enzyme 2 (ACE2) in PRCP-/- Nieren, wurde als Kompensation der fehlenden PRCP Aktivität in PRCP-/- Nieren interpretiert. bot einen Erklärungsansatz für dieses Ergebnisse. Es wird davon ausgegangen, daß ACE2 die fehlende PRCP Aktivität in knockout Mäusen kompensiert. Das es sich hierbei um eine lokale begrenzte Kompensation handeln muß, zeigten der erhöhte Blutdruck und Herzrate, sowie die milde Herzhypertrophie. Da spezifische prcp Promotoraktivität in Hirnnuclei gefunden wurde, die in die Kontrolle der Herzfrequenz und des Blutdrucks involviert sind, wird eine regulatorische Funktion von Hirnstamm-PRCP auf Herzrhytmus und Blutdruck vermutet.Prolylcarboxypeptidase (PRCP, EC3.4.16.2) is an enzyme specifically cleaving the last carboxy-terminal amino acid from substrates containing a penultimate proline. Its known potential substrates are linked to cardiovascular and metabolic phenomenon. To analyse the in vivo function of this enzyme a PRCP knockout mouse was generated. Homozygous knockout mice are viable but show tendency of decreased life span. In mice prcp expression is present in all tissues tested with very specific localizations of prcp promotor activity to distinct brain areas within the cortex, hippocampus, hypothalamus and the brain stem. The metabolic phenotype of PRCP deficient mice is characterized by low body weight even when feeding the animals a high fat diet. The increased plasma leptin levels and elevated expression of proopiomelanocortin gene (pomc) found in knockout hypothalami suggests an involvement of PRCP in the regulation of food intake and energy homeostasis. One of the gene products of pomc is alpha-melanocortin stimulating hormone (alphaMSH) that is terminating feeding when released from hypothalamic POMC neurons. Its carboxy-terminal structure is fitting the cleavage preferences of PRCP. Prcp promotor activities are localized in arcuate nucleus and paraventricular nucleus, brain areas of known alphaMSH signalling, supporting a role of PRCP in the degradation of central alphaMSH. The impact of PRCP on angiotensin II (AngII) metabolism was studied by determining the level of AngII and its degradation product Ang1-7 in blood and tissues. But instead of increased AngII levels due to the missing degradation enzyme in knockout mice, Ang1-7 levels were increased in kidney. These results were explainable by the increased activity of angiotensin converting enzyme 2 (ACE2) found in kidney. Probably ACE2 is compensating the lack of PRCP in the knockout mouse. Nevertheless, blood pressure and heart rate of PRCP knockout mice was increased. The mild hypertension was accompanied by mild hypertrophy of the hearts. Prcp promotor activity was found in brain stem an area important for regulation of blood pressure and heart rate suggesting that central PRCP regulates blood pressure.
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Sepulveda, Maria Alicia Carrillo. "Participação do receptor AT2 da angiotensina II no relaxamento vascular promovido pelo hormônio tiroideano." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-25032010-142756/.
Full textAbstract:
A vasodilatação promovida pela triiodotironina (T3) ocorre por sua ação direta sobre o relaxamento das células musculares lisas vasculares (CMLV), porém os mecanismos envolvidos são desconhecidos. Neste estudo mostramos que o T3 rapidamente relaxa as CMLV através da geração de óxido nítrico (NO), via óxido nítrico sintase neuronal e induzível (nNOS e iNOS), efeitos mediados pela sinalização PI3K/Akt. Ensaios funcionais em aortas sem endotélio, incubados com T3, mostraram menor resposta contrátil a Fenilefrina (FE), efeito este revertido pelo L-NAME, inibidor da NOS. Aortas de ratos hipertiroideos apresentaram aumento do receptor de Angiotensina II (AngII) do tipo 2 (AT2), acompanhado de diminuição de proteínas contráteis. In vitro o T3 diminui estas proteínas contráteis via AT2. Aortas sem endotélio dos ratos hipertiroideos apresentaram menor reatividade a AngII e maior relaxamento ao nitroprussiato de sódio (NPS), efeitos estes mediados via AT2. Por fim, observamos que o T3 é capaz de induzir produção de NO nas CMLV via PI3K/Akt, a qual é ativada pelo AT23,3\',5-triiodo-l-thyronine (T3) has been shown to induce vasodilation by its direct effect on vascular smooth muscle cells (VSMC). However, the mechanism by which T3 causes VSMC relaxation is still unknown. Here, we have shown that T3 causes rapid relaxation of VSMC via increased NO production from inducible and neuronal nitric oxide synthase (NOS). We further showed that these effects were mediated by PI3K/Akt signaling pathway. Vascular reactivity studies showed that endothelium-denuded aortas treated with T3 had a decreased response to phenylephrine which was reserved by L-NAME, NOS inhibitors. Aortas from hyperthyroid rats showed an upregulation of AT2 accompanied by decreased of contractile proteins. In vitro we observed that T3 decreases contractile proteins via AT2. Furthermore, endothelium-denuded aortas from hyperthyroid rats showed a decreased response to angiotensinII and augmented relaxation to sodium nitroprusside (SNP) via AT2 participation. Our data also suggests that PI3K/Akt signaling pathway is involved in T3-induced NO production in VSMC via AT2.
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Ouali, Rachida. "Caractérisation, couplage et régulation des sous-types AT1 et AT2 du récepteur à l'A-II dans les cellules fasciculo-réticulées de la surrénale bovine, en culture primaire." Lyon 1, 1994. http://www.theses.fr/1994LYO1T053.
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Fritsch, Samuel. "Rôles des récepteurs PTH des peptides dérivés de l'hormone parathyroi͏̈dienne dans l'homéostasie des systèmes cardiovasculaire et rénal." Strasbourg 1, 2004. http://www.theses.fr/2004STR13082.
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Rogers, Jennifer Leigh. "The effect of sex, growth hormone, and neuropeptide Y on early diabetic kidney disease in adult rats." Connect to Electronic Thesis (CONTENTdm), 2008. http://worldcat.org/oclc/457179712/viewonline.
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Heitzler, Domitille. "Modélisation dynamique des mécanismes de signalisation cellulaire induits par l'hormone folliculo-stimulante et l'angiotensine." Phd thesis, Université François Rabelais - Tours, 2011. http://tel.archives-ouvertes.fr/tel-00847767.
Full textAbstract:
La signalisation cellulaire induite par les r écepteurs à sept domaines transmembranaires (R7TM) contrôle les principales fonctions physiologiques humaines. Ces R7TMs sont cibles de m édicaments et initient de larges réseaux d'interactions. Nous avons modélisé dynamiquement les réseaux de signalisation du récepteur à l'hormone folliculo-stimulante (FSH) régulant la fonction de reproduction et du récepteur angiotensine, un R7TM modèle régulant la tension pour comprendre le fonctionnement de ces réseaux et prédire des données inaccessibles expérimentalement. Notre modélisation a utilisé des équations différentielles ordinaires, en assimilant une variable par espèce et un paramètre par constante cinétique. Les paramètres manquant ont été déterminés par optimisation paramétrique. Puis, nous avons d éveloppé un environnement afin de comparer plusieurs algorithmes d'optimisation et de créer une nouvelle méthode hybride plus performante et adaptée à la paramétrisation des réseaux de signalisation.
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Desarnaud, Franck. "Etude structurale des récepteurs de l'angiotensine II : purification et contribution à la cartographie du site de liaison." Montpellier 2, 1992. http://www.theses.fr/1992MON20134.
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Le present travail s'integre dans un projet visant a contribuer a l'etude des proprietes structurales et moleculaires des recepteurs de l'angiotensine 2. Une sonde biotinylee photoactivable possedant un pont disulfure dans son bras espaceur a ete concue pour le marquage covalent des recepteurs de l'angiotensine 2 et l'adsorption subsequente des complexes covalents sur avidine ou streptavidine immobilisees. Les proprietes de cette sonde ont ete etablies. Les conditions d'application de cette sonde a un protocole de purification du recepteur de foie de rat (sous-type at#1) ont ete elaborees. Sont rapportees la diversite d'utilisation de ce protocole, sa generalisation a la purification d'autres proteines ainsi que sa transposition a la purification du recepteur de type at#2. L'application de la purification et de la fragmentation du recepteur at#1 a la cartographie du site de liaison de l'hormone a permis de formuler une hypothese: le marquage covalent par la sonde implique une zone du recepteur comportant le troisieme domaine transmembranaire et les portions des boucles adjacentes. Les perspectives d'etudes de la structure tridimensionnelle du recepteur et de la cartographie de son interaction avec l'hormone sont discutees
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Welsch, Sandra. "Dérégulation de la protéine apparentée à l'hormone parathyroïde (PTHrP) et du récepteur PTH/PTHrP (récepteur PTH1) dans l'hypertension artérielle en réponse à l'angiotensine II." Université Louis Pasteur (Strasbourg) (1971-2008), 2005. https://publication-theses.unistra.fr/public/theses_doctorat/2005/WELSCH_Sandra_2005.pdf.
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Cette thèse a permis de préciser les facteurs impliqués dans la dérégulation du système PTHrP/RPTH1 dans les vaisseaux rénaux, notamment au cours de l'HTA. Mes résultats montrent que la sous-expression vasculaire rénale du R-PTH1 présente chez le SHR avec une HTA établie, est associée à une perte de la fonction vasodilatatrice rénale de la PTHrP non seulement in vitro (rein isolé perfusé) mais aussi in vivo, chez le rat anesthésié. La dérégulation du R-PTH1 apparaît comme une spécificité vasculaire rénale chez le SHR (non retrouvée sur d'autres vaisseaux, le cœur, la médulla rénale). Elle ne semble pas avoir une origine génétique (absente chez le SHR préhypertensif), mais requièrt un système rénine-angiotensine intact (réversibilité par le losartan, absence dans une HTA à rénine basse). La surexpression vasculaire rénale de la PTHrP présente les même caractéristiques (spécificité rénale, pas d'origine génétique, réversibilité par le losartan), mais répond aussi à une simple majoration de la pression artérielle. Dans la seconde partie de ce travail, j'ai confirmé sur des CMLV en culture, le rôle essentiel de l'AngII dans la dérégulation du R-PTH1 vasculaire et les mécanismes impliqués. Nos résultats montrent que l'AngII est capable d'induire une sous-expression du R-PTH1 sur des CMLV rénales provenant de rats Wistar. Elle agit en particulier en modifiant la stabilité de l'ARNm du R-PTH1 mais non en modifiant l'activité des promoteurs P1 ou P2 qui contrôlent l'activité transcriptionnelle du gène du R-PTH1. Par ailleurs, cette déstabilisation nécessite la présence de PTHrP intracrine qui semble exercer un effet synergique avec l'AngII pour déstabiliser l'ARNm du R-PTH1. Sur des CMLV rénales provenant de SHR, le système rénine-angiotensine endogène est spontanément activé. Ceci conduit à une sous-expression spontanée du R-PTH1 via une altération de la stabilité de l'ARNm du R-PTH1, et à l'absence de réponse à l'AngII exogèneThis work allowed to identify the factors involved in the dysregulation of the reno-vascular PTHrP/PTH1R system, especially during hypertension. My results show a down-regulation of renovascular PTH1R in 12 week-old SHR animals, associated with a decrease of PTHrP-induced vasodilation in vitro (isolated perfused kidney) but also in vivo, on anesthetized rats. PTH1R down-regulation seems to be a renovascular-specificity in SH rats (absent on other vessels, heart and renal medulla). This down-regulation is not a primary defect (absent in 4 weeks-old SHR) but requires an intact renin- angiotensin system (reversed by losartan, but not present in DOCA-salt induced HTA). Over-expression of reno-vascular PTHrP shows the same regulation pattern (renal specificity, not primary defect, reversed by losartan), but requires only an elevation of blood pressure. In the second part of this work, I confirm on VSMC in culture, the crucial role of AngII on vascular PTH1R down-regulation and the mechanisms that are involved. Our results shown that AngII is able to downregulate PTH1R on renal vascular smooth muscle cells (VSMC) taken from Wistar rats. AngII modified PTH1R mRNA but has no effect on either P1 or P2 promoter which control transcriptional activity of PTH1R gene. Moreover this destabilization requires intracrine PTHrP which acts in a synergistic way with AngII to destabilize PTH1R mRNA. On renal VSMC taken from SHR, the endogenous renin-angiotensin system is spontaneously activated. This leads to a spontaneously downregulation of PTH1R through stability alteration of PTH1R mRNA and to lack of response to exogenous AngII
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Penhoat, Armelle. "Caractérisation et régulation des récepteurs de l'angiotensine II dans la cellule surrénale bovine en culture primaire : rôles de l'A-II, de l'ACTH, de la somatomedine-C et de l'insuline." Lyon 1, 1987. http://www.theses.fr/1987LYO1T119.
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MOUSSEAU, MARIE-CATHERINE. "Modulation des sensibilites neuronales aux hormones angiotensine et aldosterone, ainsi qu'aux afferences gustatives eau, sel et saccharose, par des traitements agissant sur la natriophilie." Paris 6, 1997. http://www.theses.fr/1997PA066474.
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Nous avons etudie les reponses neuronales de rats vigiles soumis a deux traitements modulateurs de leur preference pour le sodium, une deshydratation et un pretraitement a la desoxycorticosterone. Une methode d'analyse statistique originale a permis de montrer que ces traitements entrainent des modifications significatives dans les sensibilites a l'angiotensine et a l'aldosterone, ainsi qu'aux stimulations gustatives salees et sucrees, au sein de groupes de neurones specifiques appartenant a la region septo-preoptique et au thalamus. Nous avons ensuite discute en quoi de telles modifications peuvent rendre compte des regulations a court terme et a long terme d'une preference gustative, et plus generalement d'un comportement.
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Derrien, Alexandrine. "Étude de la régulation des sous-unités α des protéines Gq et G11 par les hormones ACTH et AngII et de leur couplage aux récepteurs à l'angiotensine II, dans les cellules fasciculoréticulées de la surrénale bovine." Lyon 1, 1997. http://www.theses.fr/1997LYO1T019.
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Baraldi, Dhãniel Dias. "Influência do sistema renina angiotensina na modulação do estado redox, no balanço autonômico e na hipertrofia cardíaca induzida pelo hipertireoidismo experimental." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/54943.
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O hipertireoidismo é uma patologia epidemiologicamente importante, que afeta o sistema cardiovascular de forma proeminente. O estado hipertireoideo pode afetar o metabolismo basal, consumo de O2 celular, sistema renina angiotensina, assim como, estimular a produção de espécies ativas de oxigênio. Estas alterações produzem consequências morfológicas, funcionais, bioquímicas e moleculares no tecido cardíaco. A hipertrofia cardíaca, decorrente do hipertireoidismo, instala-se devido a uma série de eventos que sinalizam à proliferação e sobrevivência celular, envolvendo as espécies ativas de oxigênio, a ativação do sistema renina angiotensina cardíaco e o sistema nervoso autonômico. Neste estudo, bloqueamos o receptor AT1 da angiotensina II para avaliarmos a influência do sistema renina angiotensina cardíaco sobre o desenvolvimento da hipertrofia cardíaca, a participação do balanço autonômico sobre o coração e o papel das espécies ativas de oxigênio neste processo, em modelo experimental de hipertireoidismo. Para isto, foram utilizados ratos Wistar machos, pesando cerca de 220g, divididos em 4 grupos experimentais: Controle (C), Losartan (L) (10 mg/Kg de peso corporal/dia, 28 dias, sonda intragástrica) , T4 (12mg/L água de beber, 28 dias), e T4+L. Foram avaliados a massa cardíaca, análise espectral do balanço simpato-vagal, a expressão protéica do receptor AT1 da Angiotensina II e da gp91phox, peróxido de hidrogênio (H2O2), Nrf-2 e Heme-oxigenase-1 (HO-1) no tecido cardíaco. A hipertrofia cardíaca e o desequilíbrio autonômico induzidos pelo hipertireoidismo foram atenuados no grupo T4+L. Os níveis de H2O2, Nrf-2, gp91phox e HO-1 foram elevados no grupo T4, e significativamente reduzidos no grupo T4+L, quando comparados ao grupo Controle. A expressão protéica do receptor AT1 esteve elevada nos dois grupos hipertireoideos. Os resultados obtidos sugerem que o bloqueio do receptor AT1 promove importante impacto sobre o balanço simpato-vagal e a hipertrofia cardíaca, no hipertireoidismo, sendo as espécies ativas de oxigênio e o sistema Nrf-2/HO-1 possíveis mediadores destas alterações.Hyperthyroidism is an epidemiologic relevant pathology, which substantially affects the cardiovascular system. The hyperthyroid state may affect basal metabolism, O2 cell consumption, renin-angiotensin system, and increase reactive oxygen species production. Those alterations produce morphological, biochemical, functional and molecular consequences in cardiac tissue. Hyperthyroidism induced cardiac hypertrophy develops due to a set of events, which signals cell survival and proliferation, including reactive oxygen species, cardiac rennin-angiotensin system, and autonomic nervous system. In the present study, the role of cardiac renin-angiotensin system on development of hyperthyroidism induced cardiac hypertrophy, and the involvement of autonomic nervous system and reactive oxygen species, were assessed trough blockade of angiotensin II receptor AT1. For that, were used male Wistar rats, weighting about 220g, divided in 4 experimental groups,: Control (C), Losartan (L) (10mg/Kg body weight/day, 28 days, intragastric probe), T4 (12mg/L L-thyroxin in drinking water, 28 days), and T4+L. Cardiac mass, spectral analysis (autonomic balance), hydrogen peroxide (H2O2), and myocardial protein expression of angiotensin II receptor (AT1), NADPH oxidase, Nrf-2, and heme-oxygenase-1 (HO-1), were quantified. Cardiac hypertrophy and autonomic umbalance induced by thyroid hormones were attenuated in the T4+losartan group. The H2O2, as well as Nrf-2, gp91phox, AT1 and HO-1 immunocontent were elevated in T4 group. All these effects were attenuated by losartan, except AT1 levels. The overall results suggest that blockade of AT1 receptor lead to relevant impact on autonomic balance and cardiac hypertrophy, being ROS and Nrf-2/ HO-1 system possible mediators in this alterations in experimental hyperthyroidism.
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Custódio, Melani Ribeiro. "Avaliação do efeito isolado do fósforo e do paratormônio sobre o tecido cardíaco de ratos urêmicos paratireoidectomizados." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-11032008-155335/.
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A doença cardiovascular (DCV) é a principal causa de mortalidade nos pacientes com doença renal crônica (DRC) e a hipertrofia de ventrículo esquerdo (HVE), a alteração mais freqüente. A remodelação cardíaca (RC) patológica ocorre em resposta a agressões como sobrecarga de volume ou de pressão e é influenciada por ativação neurohormonal, fatores locais, inflamação, isquemia, necrose e apoptose celular. Os miócitos são as principais células envolvidas na RC. Avaliamos o papel da hiperfosfatemia e do paratormônio (PTH) em animais urêmicos. Trinta e dois ratos Wistar machos foram submetidos à paratireoidectomia (PTX) e nefrectomia (Nx), com reposição contínua de PTH em concentração fisiológica (PTHf= 0,022 ug/100g/h) ou elevada (PTHe=0,11 ug/100g/h). Os animais sham (N=16) foram operados e recebiam infusão de veículo. Apenas o conteúdo de fósforo nas dietas era diferente, ou seja: pobre=0,2% (pP) ou rica em fósforo=1,2% (rP). Dividimos os animais em 6 grupos: Sham: Sham-pP (G1), Sham-rP (G2); PTX+Nx: PTHf-pP (G3), PTHf-rP (G4), PTHe-pP (G5), PTHe-rP (G6). Semanalmente determinamos o peso e a pressão arterial caudal. Creatinina, fósforo, cálcio PTH e hematócrito foram analisados. Após 8 semanas os animais foram sacrificados. A hipertrofia e fibrose miocárdicas foram analisadas com o sistema digital Leica. O peso do coração corrigido por 100g peso corporal foi maior nos grupos G5 e G6 e apresentou uma correlação positiva com hipertrofia e fibrose miocárdica. A hipertrofia e fibrose foram menores no G3, quando comparado aos grupos Nx. A hipertrofia miocárdica foi maior no G6, evidenciando o papel do P neste processo. A fibrose mocárdica ocorreu principalmente em subendocárdio e foi mais intensa no G6. Analisamos a expressão do fator transformador de crescimento (TGF-beta) e angiotensina II que foram mais intensas nos grupos G5 e G6. As lesões das artérias coronarianas foram avaliadas de forma semi-quantitativa e os animais G5 e G6 mostraram calcificações de camada média. A expressão da alfa-actina se correlacionou negativamente com as lesões coronarianas. Nossos resultados demonstraram a importância do fósforo e PTH na fisiopatologia da DCV, sendo necessário um melhor controle destes elementos para prevenção de mortalidade nos pacientes com DRC.Cardiovascular disease (CVD) is the leading cause of mortality in patients with chronic kidney disease (CKD), and left ventricular hypertrophy (LVH) is the most common alteration. Pathologic cardiac remodeling (CR) occurs in response to injuries such as volume or pressure overload, and it is influenced by neurohormonal activation, local factors, inflammation, ischemia, necrosis and cellular apoptosis. Myocytes are the principal cells involved in CR. We evaluated the role of hyperphosphatemia and parathyroid hormone (PTH) in uremic animals. Thirty-two male Wistar rats were submitted to parathyroidectomy (PTX) and nephrectomy (Nx), with PTH continuous replacement in physiologic concentration (PTHf=0.022ug/100g/h) or elevated (PTHe=0.11ug/100g/h). The sham animals (N=16) were operated and received vehicle infusion. Only the phosphorus content in diets was different, that is: poor = 0.2% (pP) or rich in phosphorus = 1.2% (rP). We divided the animals into 6 groups: Sham: Sham-pP (G1), Sham-rP (G2); PTX+Nx: PTHf-pP (G3), PTHf-rP (G4), PTHe-pP (G5), PTHe-rP (G6). We determined the weight and caudal blood pressure weekly. Creatinine, phosphorus, PTH calcium and hematocrit were analyzed. After 8 weeks, the animals were sacrificed. Myocardial hypertrophy and fibrosis were analyzed using Leica digital system. The weight of the heart corrected for 100g body weight was greater in groups G5 and G6 and presented a positive correlation with myocardial hypertrophy and fibrosis. Hypertrophy and fibrosis were lower in G3, when compared to Nx groups. Myocardial hypertrophy was higher in G6, determining the role of P in this process. Myocardial fibrosis occurred mainly in subendocardium and was more intense in G6. We analyzed the expression of transforming growth factor (TGF-alfa) and angiotensin II, which were more intense in groups G5 and G6. Coronary artery lesions were evaluated semiquantitatively and G5 and G6 animals showed middle layer calcifications. Expression of alfa-actin correlated negatively with coronary lesions. Our results demonstrated the importance of phosphorus and PTH in the pathophysiology of CVD; therefore, a better control of these elements is required in order to prevent mortality in patients with CKD.
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Kabbaj, Majida Benmansour. "Applications d'une sonde biotinylée photoactivable à la caractérisation, la purification et la fragmentation du récepteur hépatique de l'angiotensine II." Montpellier 2, 1988. http://www.theses.fr/1988MON20123.
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Etude du recepteur de l'angiotensine ii du foie de rat. Cette etude comprend la determination de la structure primaire, de la topographie du site de liaison, realisee par des sondes biotinylees photoactivables
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Liu, Haiyan. "Hormonal control and pharmacology of bTREK-1 K⁺ channels in bovine adrenal zona fasciculata cells." Columbus, Ohio : Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view.cgi?acc%5Fnum=osu1245265538.
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Simon, Claude Demosthene. "Interactions between Growth Hormone and the Mechanisms Controlling Arterial Pressure and Renin Secretion in the Rat: A Thesis." eScholarship@UMMS, 1988. http://escholarship.umassmed.edu/gsbs_diss/261.
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The mechanisms whereby the pituitary gland maintains arterial pressure were investigated in rats. The arterial pressure in hypophysectomized rats was 30 mmHg below normal. Saralasin or captopril caused a further fall of 25 and 30 mmHg, respectively, suggesting that the renin-angiotensin system plays a role in blood pressure maintenance in hypophysectomized rats. Growth hormone administration to hypophysectomized rats increased the arterial pressure, but pretreatment with captopril prevented the effect. Plasma renin activity and basal renin secretion (in vitro) was normal in hypophysectomized rats despite a twofold greater renal renin content. Secretory responsiveness to isoproterenol and calcium omission was lower in hypophysectomized rats. It is concluded that the renin-angiotensin system plays a role in maintaining arterial blood pressure in hypophysectomized rats although the responsiveness of the system may be decreased.
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Lebrethon, Marie-Christine. "Régulation par les hormones (ACTH et A-II) et le facteur de croissance TGFβ1 de l'expression des gènes codant pour les fonctions différenciées des cellules fasciculo-réticulées surrénaliennes humaines." Lyon 1, 1994. http://www.theses.fr/1994LYO1T060.
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Bardoux, Pascale. "Effet albuminurique de la vasopressine chez le rat et chez l'homme : conséquences dans la néphropathie diabétique." Paris 7, 2001. http://www.theses.fr/2001PA077165.
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Nouet, Sandrine. "Contribution d'antagonistes non-peptidiques à l'étude cartographique du récepteur AT1 de l'angiotensine II." Montpellier 2, 1995. http://www.theses.fr/1995MON20038.
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Le present travail est consacre au developpement, en collaboration avec les laboratoires fournier, de sondes non-peptidiques originales tritiees et/ou photoactivables dans le cadre de l'etude cartographique du recepteur at#1 de l'angiotensine 2, plus particulierement de l'analyse topographique de son interaction avec les ligands peptidiques et non-peptidiques. La strategie suivie pour leur conception est: 1) synthese et etude des proprietes de liaison de 2 non-peptides trities: (#3h)lf7-0156 et (#3h)lf8-0129 qui ont de plus permis d'evaluer l'incidence de mutations du recepteur sur la reconnaissance des non-peptides, 2) synthese des 2 derives photoactivables non-radioactifs, susceptibles de marquer des zones distinctes du recepteur, demonstration de la superiorite de l'un des 2, lf13-0023, a marquer irreversiblement les sites recepteurs, 3) synthese de la sonde photoactivable tritiee (#3h)lf13-0023, demonstration de son aptitude a photomarquer le recepteur at#1 recombinant exprime dans les cellules cho, avec un rendement eleve (10%). Sont proposees des etapes de purification partielle des complexes covalents non-peptide/recepteur qui permettront leur fragmentation et la comparaison des profils de fragmentation avec ceux obtenus avec des sondes peptidiques ; la perspective est d'obtenir des informations directes en faveur ou a l'encontre de points d'interaction communs du recepteur avec les 2 types de ligands. Il est prevu d'integrer les donnees biochimiques et de mutagenese dirigee dans l'elaboration de modeles d'interaction des ligands peptidiques et non-peptidiques avec le recepteur at#1
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Dauphin-Villemant, Chantal. "Etude du fonctionnement de l'interrenale (corticosurrenale) chez la femelle du lezard vivipare jacquin : evolution au cours du cycle annuel d'activite et de reproduction." Paris 6, 1987. http://www.theses.fr/1987PA066329.
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Lihrmann, Isabelle. "Rôle du calcium dans les processus de couplage stimulus-sécrétion dans la cellule corticosurrénalienne chez les amphibiens." Rouen, 1986. http://www.theses.fr/1986ROUES040.
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Au moyen de deux techniques complémentaires, la périfusion de fragments de surrénales et le dosage radioimmunologique des corticostéroïdes et des prostaglandines, l'auteur montre que les concentrations croissantes de calcium stimulent la corticostéroïdogénèse. L'importance du calcium extracellulaire et intracellulaire a été évaluée par le biais d'agents pharmacologiques bloquant l'entrée de calcium dans la cellule ou inhibant les mouvements de calcium intracellulaire. Le calcium extracellulaire est nécessaire au maintien de la stéroïdogénèse spontanée ainsi qu'à l'action de l'ACTH. Au contraire, il n'intervient presque pas dans le mécanisme d'action de l'angiotensine; celui-ci dépend essentiellement d'une libération de calcium à partir d'un compartiment intracellulaire, vraisemblablement, le réticulum endoplasmique. Dans le mécanisme d'action de l'ACTH, le calcium extracellulaire est essentiel soit pour la liaison de l'hormone à son récepteur, soit pour la transduction du message hormonal entre le complexe hormone-récepteur et la sous-unité catalytique de l'adénylate cyclase. Dans le mécanisme d'action de l'angiotensine qui implique non pas une formation d'AMPC, mais une synthèse de prostaglandines, le calcium intracellulaire semble être mobilisé au cours des étapes qui suivent la formation de prostaglandines. Le calcium extracellulaire est également nécessaire à l'action corticotrope de l'acétylcholine. Par ailleurs, l'absence de calcium dans le milieu de périfusion inhibe la synthèse de prostaglandines stimulée par l'acétylcholine. En conclusion, le rôle du calcium est crucial dans la réponse des cellules corticosurrénaliennes à l'ACTH, à l'angiotensine et à l'acétylcholine chez les amphibiens, bien que l'étape sur laquelle le calcium agit soit différente dans chacun des trois cas. Par ailleurs cette étude souligne l'étroite relation existant entre le système messager "calcium" et certains métabolites de l'acide arachidonique
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Alves, Julio Cesar Santana. "Influência de hormônios gonadais no eixo [ECA2/ANG(1-7)/Mas] encefálico para o controle da sede e apetite por sódio em ratos." Universidade Federal de Sergipe, 2013. https://ri.ufs.br/handle/riufs/3870.
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Sodium and water intake are important regulatory components of the hidromineral balance. In this context, human body regulates hidromineral imbalance through the neuro-immune-endocrine and behavioral response. Gonadal hormones are important players for the modulation of ingestive behaviors. The present study aimed to investigate the influence of male and female gonadal hormones in cerebral ECA2/ANG-(1-7)/Mas axis over the control of water sodium intake in rats. In this experiment, ovariectomized female rats were treated with estradiol benzoate (20μg/animal/day, sc; OVXE) or vehicle (sunflower oil; OVXV). Male rats underwent bilateral orchiectomy (ORQX) or sham surgery (SHAM). Guide cannulae were implanted into the right lateral ventricle for intracerebroventricular administration (icv) of drugs. We used angiotensin-converting enzyme type 2 (ACE2) activator, DIZE (diminazene of aceturate, 40 nmol / 2μl , icv ) or the antagonist of Ang-(1-7) Mas recetor, D-Ala7-ANG-(1-7) (A779, 10 nmol / 2μl, icv). The vehicle for both drugs was artificial cerebrospinal fluid (aCFS) administered in the same volume. For induction of thirst and sodium appetite, animals were subjected to hydrossaline depletion by administration of furosemide (20 mg / kg, sc) and access to distilled water and low sodium diet (corn ) for 24 hours. After microinjection of drugs, water and 0.3 M NaCl were reoffered and the ingested volume were recorded at the following 15, 30 , 60, 90 , 120, 180, 240 min and 24 h. Two-way analysis of variance was performed, followed by Bonferroni posthoc test when appropriate. The level of significance was p < 0.05. In females treated with vehicle or DIZE, sodium and water intake, as well as sodium preference index (SPI) did not differ between groups. However, OVXV ingested less water than OVXE when both were treated with A779 (p < 0.05). Twenty-four hours after reintroduction of fluids intake sodium ingestions was higher in OVXV than in OVXE when both received A779 (p<0.05). Similarly, OVXV rats showed greater preference for sodium when compared to OVXE, if both received icv injection of A779. Males ORQX microinjected with aCFS ingested more water than SHAM+aCSF. However, at 30 min, SHAM+DIZE male rats presented higher water intake when compared to their respective control. Up to 15 min after reintroduction of fluids, ORQX rats ingested less sodium than SHAM rats, regardless DIZE administration (p < 0.05). Water intake as well as SPI did not differ between groups in males undergoing A779 administrarion. However sodium intake was lower in ORQX+A779 than in ORQX+aCFS (p < 0.05) at 30, 60 , 90, 120 , 180 and 240 min after fluid presentation. Thus, we conclude that estrogen seems to exert inhibitory influences on sodium intake independent ECA2/ANG (1-7)/Mas activity. On the other hand, the male gonadal hormones act by raising intake for the regulation of salt intake shaft in the proposed protocol.Os comportamentos de ingestão de sódio e água constituem importantes componentes regulatórios do equilíbrio hidroeletrolítico. Neste contexto, o organismo humano regula seu déficit hidromineral através de uma resposta neuroimunoendócrina e comportamental comandada majoritariamente pelo sistema nervoso central (SNC). Reconhecidamente, os hormônios gonadais representam importantes fatores moduladores dos comportamentos ingestivos. O presente estudo objetivou estudar a influência dos hormônios gonadais masculinos e femininos no eixo ECA2/ANG(1-7)/Mas sobre o controle da ingestão de água e NaCl 0,3 M em ratos e ratas. Neste experimento, fêmeas ovariectomizadas foram tratadas com benzoato de estradiol (20μg/animal/dia, s.c.; OVXE), ou com veículo (óleo de girassol; OVXV). Machos foram submetidos à orquiectomia bilateral (ORQX) ou cirurgia fictícia (SHAM). Por meio de cirurgia estereotáxica, cânulas-guia foram implantadas no ventrículo lateral direito para administração intracerebroventricular (icv) das drogas utilizadas. Foram utilizados o ativador da enzima conversora de angiotensina tipo 2 (ECA2), DIZE (Aceturato de Diminazeno, 40 nmol / 2 μL, i.c.v.) ou o antagonista do receptor Mas de ANG (1-7), o D-Ala7-ANG(1-7) (A779, 10 nmol / 2 μL, i.c.v.). O veículo para ambas as drogas foi líquido cerebro-espinhal artificial (LCEa), administrado nos animais controle em igual volume. Para indução da sede e apetite por sódio, os animais foram submetidos a depleção hidrossalina por administração de um diurético de alça (furosemida, 20 mg / kg, s.c.) e acesso à água destilada e dieta pobre em sódio (fubá de milho) por 24 horas. Após a microinjeção das drogas, água e de NaCl 0,3 M foram reapresentados e registrados os volumes ingeridos nos tempos 15, 30, 60, 90, 120, 180, 240 min e 24 h. Foram realizadas análises de variância de duas vias seguidas do pós-teste de Bonferroni, quando necessário. O nível de significância foi de p < 0,05. Os dados demonstraram que, em fêmeas tratadas com DIZE ou veículo, a ingestão de água, NaCl 0,3 M e o índice de preferência ao sódio (IPS) não diferiram entre os grupos. Porém, fêmeas OVXV ingeriram menos água quando comparadas às femeas OVXE, quando ambas foram tratadas com A779 (p < 0,05). Vinte e quatro horas após a reapresentação de fluidos, a ingestão de NaCl 0,3 M foi maior em ratas OVXV que nas OVXE, quando ambas receberam A779 (p < 0,05). No mesmo sentido, ratas OVXV apresentaram maior preferência por sódio que as OVXE, ambas tratadas com A779. Machos ORQX microinjetados com LCEa ingeriram mais água quando comparados aos animais do grupo SHAM+LCEa. Todavia, aos 30 min, os machos SHAM+DIZE apresentaram maior ingestão de água quando comparado ao seu respectivo controle. Até 15 min após a reapresentação de fluidos, a ingestão de NaCl 0,3 M em ratos ORQX foi menor em comparação aos ratos SHAM independente do tratamento com DIZE (p<0,05), o IPS não diferiu entre os grupos. Os dados referentes a ingestão de água e ao IPS em machos submetidos ao tratamento icv com A779, revelam não haver diferença entre os grupos estudados, porém para ingestão de NaCl 0,3 M, os ratos ORQX+A779 demonstraram menor ingestão quando comparados aos animais ORQX+LCEa (p<0,05) nos tempos 30, 60, 90, 120, 180 e 240 min. Assim, podemos concluir que o estrógeno parece exercer influencia inibitória na ingestão de sódio independente da atividade do eixo ECA2/ANG(1-7)/Mas. Por outro lado, os hormônios gonadais masculinos atuam elevando a ingestão hidrossalina para a regulação do eixo no protocolo proposto.
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Mandel, Philipp [Verfasser], Nicole [Gutachter] Schupp, and Ulrike [Gutachter] Holzgrabe. "Entstehung von oxidativen Stressmarkern in DNA und RNA nach der Behandlung mit den Hormonen Angiotensin II und Aldosteron in vitro und in vivo : Vergleich von drei Analysemethoden zum Nachweis von 8-Oxo-2'-desoxyguanosin in LLC-PK1-Zellen / Philipp Mandel. Gutachter: Nicole Schupp ; Ulrike Holzgrabe." Würzburg : Universität Würzburg, 2015. http://d-nb.info/1109750323/34.
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Mandel, Philipp. "Entstehung von oxidativen Stressmarkern in DNA und RNA nach der Behandlung mit den Hormonen Angiotensin II und Aldosteron in vitro und in vivo : Vergleich von drei Analysemethoden zum Nachweis von 8-Oxo-2'-desoxyguanosin in LLC-PK1-Zellen." Doctoral thesis, 2014. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-111190.
Full textAbstract:
The detection of oxidative stress markers has gained increasing importancy in the early investigation of diseases like diabetes, cancer or hypertension. 8 oxo 2' deoxyguanosine (8-oxodG) is the main marker, which is used for the intracellular detection of oxidative stress levels. However, the oxidative stress markers 8 oxoguanine (8-oxoGua), a product of the DNA base excision repair and 8 oxoguanosine (8-oxoGuo), a marker for oxidative damaged RNA have received less attention up to now. The renin-angiotensin-aldosterone system (RAAS) plays an important role in the regulation processes of the blood pressure system. During hypertension angiotensin II (Ang II) and aldosterone (Aldo) are released in high concentrations over a longer period leading to non-physiological effects of the RAAS hormones. Subsequently, an increase of the intracellular oxidative stress level in kidney cells can be measured. The aim of this thesis is the in vitro and in vivo detection of the oxidative damage in DNA and RNA by measuring oxidative stress markers, especially 8-oxodG which is triggered by Ang II and Aldo. In vitro experiments were carried out in LLC-PK1, a cell line originated from porcine kidney cells. It could been shown that Ang II and Aldo led to a dose-dependent increase of DNA damage in the cells. A time-dependent increase was detected for the first 30 minutes of the treatment. For the rest of the experimental set up (4 h) the level of detected DNA damage remained constant. The FPG comet assay and the immunocytochemical staining showed a significant increase of 8-oxodG in the cells, whereas the HPLC-MS/MS measurement only detected a small increase of 8-oxodG in the DNA. The FPG enzyme, which recognises also other oxidized purines besides 8-oxodG, which led to an overestimation of 8-oxodG in the comet assay. Also, the 8 oxodG antibody, which was used in the immunocytochemical analysis, detected higher amounts of 8-oxodG most likely due to its side reactions with other oxidized DNA structures. One of the main advantages of the last mentioned methods is the direct measurement in damaged cells, whereas the HPLC-MS/MS requires an isolation of the DNA. During this isolation process the oxidative stress markers can be oxidized and the detection can become imprecise. The main purpose of the in vivo experiments was the detection of the oxidative stress marker 8-oxoGua, 8-oxodG and 8-oxoGuo in the urine of test animals. The treatment of C57BL/6 mice and Sprague Dawley (SD) rats with the RAAS hormones led to an increase of the blood pressure, higher DNA damage due to oxidative stress as well as an increased excretion rate of oxidative stress markers. The inhibition of the angiotensin II type 1- or mineralocorticoid receptor and a mutation of the AT1a gene could show, that the DNA damage is independent from the hypertension. In addition, it was shown that the NOX4 is not alone responsible for the oxidative stress. Other NADPH oxidases must contribute to the induction of oxidative stress inside the cell. Moreover, the activation of the Nrf2 pathway has an influence on the effect of Aldo in SD rats. The excretion rate of the oxidative stress markers in the 20 h urine of the treated animals showed how the equilibrium between the DNA repair and the oxidative stress level was changing over time. The measurement of 8-oxoGuo became more and more popular, because up to the fact that 80 % of the DNA is translated into RNA. Overall, the detection of 8-oxodG and 8-oxoGuo is feasible for monitoring the disease or the healing process, because the measurement is non-invasive. The detection of 8-oxodG and 8-oxoGuo in nucleic acids is a first step into the field of basic research methods, because it reveals a snapshot of the nucleic acid damage in the cell at a specific time point. Usually, there will be an overestimation of the oxidative stress marker resulting from the analytical method. Although, it is possible to detect an underestimation of oxidative stress markers in tissue samples if not all cell types are damaged equally. Therefore, a primary goal should be the detection of a stable oxidation product of guanine to insure a reliable detection strategy and for a better understanding of the equilibrium of DNA oxidation and repairDer Nachweis von oxidativen Stressmarkern hat bei der Untersuchung von Krankheiten wie Diabetes, Krebs und Hypertonie an großer Bedeutung gewonnen. Vor allem 8-Oxo-2’-desoxyguanosin (8-oxodG) wird gezielt mit verschiedenen Methoden gemessen und als Marker für oxidativen Stress herangezogen. Daneben haben 8 Oxoguanin (8-oxoGua), als Produkt aus der Basenexzisionsreparatur der DNA, sowie 8-Oxoguanosin (8-oxoGuo), als Biomarker für oxidativ geschädigte RNA, bisher weniger Aufmerksamkeit bekommen. Das Renin-Angiotensin Aldosteron System (RAAS) spielt eine wichtige Rolle in der Regulierung des Blutdrucks. Im Falle einer Hypertonie werden Angiotensin II (Ang II) und Aldosteron (Aldo) über einen langen Zeitraum in erhöhter Konzentration ausgeschüttet. Dieser Umstand bewirkt eine nicht physiologische Wirkung der Hormone des RAAS, welche zu einer Induktion von oxidativem Stress führt. Die Zielsetzung dieser Arbeit ist es, die oxidative Schädigung, ausgelöst durch Ang II und Aldo, in der DNA und der RNA in vitro und in vivo nachzuweisen und dabei speziell den Biomarker 8-oxodG zu untersuchen. In-vitro-Experimente wurden mit LLC PK1-Zellen, einer Schweinenierenzelllinie, durchgeführt. Ang II und Aldo lösten einen dosisabhängigen Anstieg der DNA Schäden in LLC PK1 Zellen aus. Eine Zeitabhängigkeit wurde für die ersten 30 Minuten gezeigt. Für die restliche Zeit (4 h) blieb der nachgewiesene DNA Schaden konstant. Der FPG Comet-Assay und die immunzytochemische Färbung zeigten jeweils eine signifikante Zunahme von 8-oxodG in LLC-PK1-Zellen an, während die HPLC MS/MS Messung nur geringe Veränderungen nachwies. Das FPG Enzym erkennt neben 8-oxodG auch andere oxidierte Purine und sorgte so für eine Überbestimmung des DNA-Schadens. Bei der immunzytochemischen Färbung entsteht die Überbestimmung durch Kreuzreaktionen des 8 oxodG Antikörpers mit oxidierten Strukturen in der DNA. Der Vorteil beider Analysemethoden ist die direkte Messung von Schädigungen in der Zelle, während die HPLC-MS/MS eine Isolierung der Nukleinsäuren voraussetzt. Bei diesem Schritt kann es zur Oxidation der Marker für oxidativen Stress kommen, welche einen genauen Nachweis erschwert. In vivo-Versuche hatten zum Ziel, die oxidativen Stressmarker 8-oxoGua, 8-oxodG und 8-oxoGuo im Urin nachzuweisen. Die Behandlung der C57BL/6-Mäuse und Sprague Dawley-Ratten (SD-Ratten) mit den Hormonen des RAAS zeigten einen Anstieg des Blutdrucks, erhöhte DNA Schäden durch oxidativen Stress sowie erhöhte Exkretionsraten der oxidativen Stressmarker. Durch eine Inhibierung des Angiotensin II-Typ1- oder Mineralkortikoidrezeptors sowie die Mutation des Gens AT1a konnte gezeigt werden, dass die Schädigungen unabhängig vom Blutdruck sind. Zudem konnte gezeigt werden, dass neben NOX4 auch andere NADPH Oxidasen für den oxidativen Stress verantwortlich sein müssen. Eine Aktivierung des Nrf2 Signalweges in den SD-Ratten hat Einfluss auf die Wirkung von Aldo. Die Exkretionsrate der oxidativen Biomarker im 20-h-Urin der behandelten Tiere zeigen, wie sich das Gleichgewicht zwischen DNA-Reparatur und oxidativem Stress verändert. Da 80 % der DNA in RNA umgeschrieben werden, ist der Nachweis von 8 oxoGuo in den Fokus gerückt. In der praktischen Anwendung kann mit der Messung von 8 oxodG und 8-oxoGuo ein Krankheits- oder Heilungsprozess auf nicht invasive Weise verfolgt werden. Der Nachweis von 8-oxodG und 8-oxoGuo in den Nukleinsäuren stellt einen Einstieg für die Grundlagenforschung dar, da sie nur eine Momentaufnahme der Nukleinsäureschädigung in der Zelle zeigen. Meist findet eine Überbestimmung, ausgelöst durch die Messmethode, statt. In Gewebeproben kann eine Unterbestimmung vorliegen, falls nicht alle Zelltypen vom oxidativen Stress betroffen sind. Daher sollte es ein vorrangiges Ziel sein, ein stabileres Oxidationsprodukt des Guanins nachzuweisen, um das Gleichgewicht der DNA-Oxidation und Reparatur besser zu verstehen
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Klug, Eric Quinton. "The effect of perindopril, a new angiotensin converting enzyme inhibitor on the hormonal response to brisk exercise in healthy subjects." Thesis, 1994. https://hdl.handle.net/10539/24495.
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A dissertation submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg, for the Degree of Master of Medicine. Johannesburg 1994.Cardiovascular drugs have varying effects on haemodynamic, metabolic, and hormonal responses to exercise. Angiotensin converting enzyme inhibitors (ACEI) have been used for the treatment of systemic hypertension, left ventricular dysfunction with or without congestive heart failure, and increasingly, for occlusive coronary artery disease and its complications..
IT2018
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Beavers, Keith. "Investigating the efficacy of the NASA fluid loading protocol for astronauts: The role of hormonal blood volume regulation in orthostasis after bed rest." Thesis, 2009. http://hdl.handle.net/10012/4532.
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Despite years of research, the role that hypovolemia plays in orthostatic intolerance after head down bed rest (BR) and spaceflight remains unclear. Additionally, the efficacy of oral saline countermeasures, employed in an attempt to restore plasma volume (PV) after BR is questionable. Several previous studies have suggested that a new homeostatic set point is achieved in space or during BR, making attempts to restore PV temporary at best. We tested the hypotheses that one day of BR would induce a transient increase in PV followed by hypovolemia and new hormonal balance; that a salt tablet and water fluid loading (FL) countermeasure would be ineffective in restoring PV; and also that the FL would not attenuate the exaggerated hormonal responses to orthostatic stress that are expected after 28hr of BR. Plasma volume, serum sodium and osmolarity, and plasma ANP, AVP, renin, angiotensin II, aldosterone, and catecholamines were measured in nine male subjects undergoing 5 different protocols (28hr Bed Rest without Fluid Loading = 28NFL, 28hr Bed Rest with Fluid Loading = 28FL, 4hr Seated Control = 4NFLS, 4hr Seated Control with Fluid Loading = 4FLS, and 4hr Bed Rest = 4BR) in a randomized repeated measures design. The FL countermeasure was 15 ml/kg of body weight of water with 1g of NaCl per 125ml of water. Orthostatic testing by lower body negative pressure (LBNP) was performed before and after all protocols. In agreement with our first hypothesis, we observed transient reductions in renin, angiotensin II, and aldosterone, which after 25.5hr were restored to baseline, slightly augmented, and suppressed, respectively. Also after 25.5hr, PV was reduced in the 28hr BR protocols and was not restored in 28FL; however, the FL protocol increased PV during 4FLS. We additionally observed augmented renin and aldosterone responses, as well as generally elevated angiotensin II after 28NFL, but not after 28FL or any of the 4hr protocols. Furthermore, no changes in plasma norepinephrine responses to LBNP were documented from Pre-Post test in any protocol. Our results indicate that: 1) PV is reduced after short term BR and is not restored by an oral FL; 2) renin-angiotensin-aldosterone system (RAAS) responses to orthostatic stress are augmented after 28hr of BR and the amplified response can be abrogated by FL; and 3) plasma norepinephrine responses during orthostatic stress are not affected by BR or FL, suggesting that RAAS activity may be modulated by FL independently of sympathetic activity and PV during orthostasis after bed rest.