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Relevant bibliographies by topics / Angiotensins. Hormones

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Academic literature on the topic 'Angiotensins. Hormones'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "Angiotensins. Hormones"

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Noureddine, Fatima Y., Raffaele Altara, Fan Fan, Andriy Yabluchanskiy, George W. Booz, and Fouad A. Zouein. "Impact of the Renin–Angiotensin System on the Endothelium in Vascular Dementia: Unresolved Issues and Future Perspectives." International Journal of Molecular Sciences 21, no. 12 (June 16, 2020): 4268. http://dx.doi.org/10.3390/ijms21124268.

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The effects of the renin–angiotensin system (RAS) surpass the renal and cardiovascular systems to encompass other body tissues and organs, including the brain. Angiotensin II (Ang II), the most potent mediator of RAS in the brain, contributes to vascular dementia via different mechanisms, including neuronal homeostasis disruption, vascular remodeling, and endothelial dysfunction caused by increased inflammation and oxidative stress. Other RAS components of emerging significance at the level of the blood–brain barrier include angiotensin-converting enzyme 2 (ACE2), Ang(1–7), and the AT2, Mas, and AT4 receptors. The various angiotensin hormones perform complex actions on brain endothelial cells and pericytes through specific receptors that have either detrimental or beneficial actions. Increasing evidence indicates that the ACE2/Ang(1–7)/Mas axis constitutes a protective arm of RAS on the blood–brain barrier. This review provides an update of studies assessing the different effects of angiotensins on cerebral endothelial cells. The involved signaling pathways are presented and help highlight the potential pharmacological targets for the management of cognitive and behavioral dysfunctions associated with vascular dementia.

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Bernardi, Stella, Barbara Toffoli, Federica Tonon, Morena Francica, Elena Campagnolo, Tommaso Ferretti, Sarah Comar, Fabiola Giudici, Elisabetta Stenner, and Bruno Fabris. "Sex Differences in Proatherogenic Cytokine Levels." International Journal of Molecular Sciences 21, no. 11 (May 29, 2020): 3861. http://dx.doi.org/10.3390/ijms21113861.

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Background: It has been shown that sex affects immunity, including cytokine production. Given that atherosclerosis is an inflammatory disease promoted by specific cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, we aimed at evaluating whether sex could affect the levels of these proatherogenic cytokines in a group of healthy adults. In this analysis, we also included other cytokines and peptides that have been implicated in atherosclerosis development and progression. Methods: A total of 104 healthy adults were recruited; we measured circulating levels of IL-1β, IL-6, TNF-α, angiotensins and angiotensin-converting enzyme-2 (ACE2), as well as osteoprotegerin and receptor activator of nuclear factor κB ligand (RANKL). Results: IL-1β, IL-6, and TNF-α were significantly higher in men as compared to women. They were all associated with testosterone and the testosterone/estradiol ratio. They remained significantly associated with sex (but not with hormones) after being tested for potential confounders. Conclusions: Sex seems to influence the levels of proatherogenic cytokines. This is consistent not only with sex differences in vulnerability to infections but also with the higher cardiovascular risk exhibited by the male gender as compared to the female gender. Nevertheless, this association is only partly explained by hormone levels.

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Pandey, K. N., and T. Inagami. "Regulation of renin angiotensins by gonadotropic hormones in cultured murine Leydig tumor cells. Release of angiotensin but not renin." Journal of Biological Chemistry 261, no. 9 (March 1986): 3934–38. http://dx.doi.org/10.1016/s0021-9258(17)35604-1.

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Galán-Ocaña, A., M. J. Ramírez-Expósito, J. M. Martínez-Martos, S. Tellado, and C. Azorit. "Regulation of aminopeptidases by the renin - angiotensin system: monitoring seasonal variations in red deer and fallow deer from a Mediterranean ecosystem." Animal Production Science 52, no. 8 (2012): 761. http://dx.doi.org/10.1071/an12023.

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The circulating renin–angiotensin system (RAS) is well known for its systemic role in the regulation of blood pressure, renal hemodynamics and fluid homeostasis. However, in mammals several organs also contain a local RAS, including male and female reproductive tissues. In the present study we analysed serum from a free-living population of red deer (Cervus elaphus hispanicus) and fallow deer (Dama dama) to determine the activity of four RAS-regulating aminopeptidases (aminopeptidase A, aspartyl aminopeptidase, aminopeptidase N and aminopeptidase B) as part of a study of annual cycles of growth and condition. Our aim was to detect seasonal variations in the activities of these aminopeptidases and their relationship to the reproductive behaviour of both species in a Mediterranean environment. In both males and females there was a maximum peak of activity in autumn. A second peak was detected in spring for males while in females activity was also higher in summer. These changes may be related to a different endocrine status according to their seasonal cycle, the decreased photoperiod in autumn and the normal timing of the seasonal growth cycle. Thus, changes in the activity of RAS-regulating aminopeptidases could reflect the functional role of angiotensins through the annual cycle of both species, also suggesting an important role of these peptide hormones in the regulation of these biological processes.

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Takei, Yoshio, Ippei Suzuki, Marty K. S. Wong, Ryan Milne, Simon Moss, Katsufumi Sato, and Ailsa Hall. "Development of an animal-borne blood sample collection device and its deployment for the determination of cardiovascular and stress hormones in phocid seals." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 311, no. 4 (October 1, 2016): R788—R796. http://dx.doi.org/10.1152/ajpregu.00211.2016.

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An animal-borne blood sampler with data-logging functions was developed for phocid seals, which collected two blood samples for the comparison of endocrinological/biochemical parameters under two different conditions. The sampler can be triggered by preset hydrostatic pressure, acceleration (descending or ascending), temperature, and time, and also manually by light. The sampling was reliable with 39/50 (78%) successful attempts to collect blood samples. Contamination of fluids in the tubing to the next blood sample was <1%, following the prior clearance of the tubing to a waste syringe. In captive harbor seals ( Phoca vitulina), the automated blood-sampling method was less stressful than direct blood withdrawal, as evidenced by lower levels of stress hormones ( P < 0.05 for ACTH and P = 0.078 for cortisol). HPLC analyses showed that both cortisol and cortisone were circulating in seal blood. Using the sampler, plasma levels of cardiovascular hormones, atrial natriuretic peptide (ANP), AVP, and ANG II were compared in grey seals ( Halichoerus grypus), between samples collected when the animals were on land and in the water. HPLC analyses determined that [Met12] ANP (1–28) and various forms of angiotensins (ANG II, III, and IV) were circulating in seal blood. Although water immersion profoundly changes the plasma levels of cardiovascular hormones in terrestrial mammals, there were only tendencies toward an increase in ANP ( P = 0.069) and a decrease in AVP ( P = 0.074) in the seals. These results suggest that cardiovascular regulation in phocid seals may have undergone adaptation during evolution of the carnivore to a semiaquatic lifestyle.

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Clapp, Carmen, Stéphanie Thebault, Michael C. Jeziorski, and Gonzalo Martínez De La Escalera. "Peptide Hormone Regulation of Angiogenesis." Physiological Reviews 89, no. 4 (October 2009): 1177–215. http://dx.doi.org/10.1152/physrev.00024.2009.

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It is now apparent that regulation of blood vessel growth contributes to the classical actions of hormones on development, growth, and reproduction. Endothelial cells are ideally positioned to respond to hormones, which act in concert with locally produced chemical mediators to regulate their growth, motility, function, and survival. Hormones affect angiogenesis either directly through actions on endothelial cells or indirectly by regulating proangiogenic factors like vascular endothelial growth factor. Importantly, the local microenvironment of endothelial cells can determine the outcome of hormone action on angiogenesis. Members of the growth hormone/prolactin/placental lactogen, the renin-angiotensin, and the kallikrein-kinin systems that exert stimulatory effects on angiogenesis can acquire antiangiogenic properties after undergoing proteolytic cleavage. In view of the opposing effects of hormonal fragments and precursor molecules, the regulation of the proteases responsible for specific protein cleavage represents an efficient mechanism for balancing angiogenesis. This review presents an overview of the actions on angiogenesis of the above-mentioned peptide hormonal families and addresses how specific proteolysis alters the final outcome of these actions in the context of health and disease.

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Goligorsky, M. S., D. Osborne, T. Howard, K. A. Hruska, and I. E. Karl. "Hormonal regulation of gluconeogenesis in cultured proximal tubular cells: role of cytosolic calcium." American Journal of Physiology-Renal Physiology 253, no. 5 (November 1, 1987): F802—F809. http://dx.doi.org/10.1152/ajprenal.1987.253.5.f802.

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Gluconeogenic competence of primary cultures of canine renal proximal tubular cells has been examined. Cells grown in 5 mM glucose media or in glucose-free media exhibited pyruvate-stimulated glucose production, as opposed to cells grown in 20 mM glucose media. By 72 h after the last media change, confluent cells grown in 5 mM glucose medium turn from a predominantly glycolytic to an oxidative type of metabolism. By this time, glucose production exhibited pH, 3-mercaptopicolinate, and insulin sensitivity. Parathyroid hormone, angiotensin II, and phenylephrine stimulated glucose production in a nonadditive fashion. Single-cell cystolic Ca2+ measurements using microspectrofluorometric techniques revealed that all three hormones elicited Ca2+ transients in proximal tubular cells. Ionomycin stimulated glucose production by proximal tubular cells, suggesting that Ca2+ transients could represent a sufficient stimulus for glucose production. When hormone-induced Ca2+ transients were curtailed by a pretreatment with the membrane-permeant Ca2+ chelator, Maptam, hormonal stimulation of glucose production was abolished, suggesting that Ca2+ transients represent not only a sufficient, but a necessary event in the stimulation of glucose production by these hormones.

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Siqueira, Lucas C., Joabel T. dos Santos, Rogério Ferreira, Robson Souza dos Santos, Adelina M. dos Reis, João F. Oliveira, Joanne E. Fortune, and Paulo Bayard Gonçalves. "Preovulatory changes in the angiotensin II system in bovine follicles." Reproduction, Fertility and Development 25, no. 3 (2013): 539. http://dx.doi.org/10.1071/rd11316.

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The present study evaluated whether the gonadotrophin surge modulates components of the renin–angiotensin system and whether angiotensin II (Ang II) plays a role in the production of hormones by follicular cells during the ovulatory process. In Experiment 1, cows were ovariectomised at various times (0, 3, 6, 12 and 24h) after GnRH injection to obtain preovulatory follicles. The concentration of Ang II in follicular fluid increased after GnRH and reached a peak at 24h, concomitant with the peak of angiotensinogen (AGT) mRNA expression in granulosa cells. AGT mRNA was not expressed in theca cells. Ang II receptor type 2 and angiotensin-converting enzyme mRNA levels were transiently upregulated in theca cells. In Experiment 2, an in vitro culture was used to determine whether Ang II could modulate hormone production by healthy dominant follicles. In the absence of LH, Ang II did not alter hormonal production by either theca or granulosa cells. Ang II plus LH increased progesterone and prostaglandin secretion by granulosa cells. In summary, the renin–angiotensin system is actively controlled during the preovulatory period and Ang II amplifies the stimulatory effects of LH on the secretion of progesterone and prostaglandins by granulosa cells.

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Pfeilschifter, J., A. Kurtz, and C. Bauer. "Role of phospholipase C and protein kinase C in vasoconstrictor-induced prostaglandin synthesis in cultured rat renal mesangial cells." Biochemical Journal 234, no. 1 (February 15, 1986): 125–30. http://dx.doi.org/10.1042/bj2340125.

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It was the aim of the present study to find out if a common mechanism exists by which the vasoconstrictive hormones angiotension II, noradrenaline and 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (AGEPC) increase prostaglandin E2 (PGE2) synthesis in cultures of rat renal mesangial cells. Angiotension II, noradrenaline and AGEPC stimulated PGE2 synthesis and uptake of 45Ca2+ in cultured mesangial cells. Both of these effects could be completely suppressed by the calcium channel blocker verapamil. Angiotensin II, noradrenaline and AGEPC caused a rapid breakdown of phosphatidylinositol 4,5-bisphosphate with a concomitant increase of 1,2-diacylglycerol and inositol trisphosphate, indicating an activation of phospholipase C by these hormones. Addition of verapamil had no effect on the hormone-induced stimulation of phospholipase C. The synthetic analogue of diacylglycerol, 1-oleoyl-2-acetylglycerol, and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), both of which are known to stimulate protein kinase C, enhanced PGE2 synthesis. Chelation of extracellular calcium with EDTA or addition of verapamil abolished the effect of 1-oleoyl-2-acetylglycerol and phorbol ester on PGE2 synthesis. 1-Oleoyl-2-acetylglycerol and phorbol ester increased the uptake of 45Ca2+ by the cells in a dose-dependent manner and this effect could be blocked by verapamil. The entirety of these data leads us to suggest that vasoconstrictor-evoked synthesis of PGE2 in rat mesangial cells is mediated by the subsequent activation of phospholipase C and protein kinase C. The activation of protein kinase C by diacylglycerol is likely to be involved in the increase of the calcium permeability of the plasma membrane which is a prerequisite for PGE2 synthesis induced by vasoconstrictive hormones.

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Ferlazzo, Adriana, Cristina Cravana, Esterina Fazio, and Pietro Medica. "The different hormonal system during exercise stress coping in horses." May-2020 13, no. 5 (2020): 847–59. http://dx.doi.org/10.14202/vetworld.2020.847-859.

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The review discusses the hormonal changes during exercise stress. The exercise generally produces a rise of adrenaline (A), noradrenaline (NA), adrenocorticotropic hormone (ACTH), cortisol, glucagon, growth hormone, arginine vasopressine, etc., and a drop of insulin. The hormonal events during reestablishment of homeostasis due to exercise stress can be divided into a catabolic phase, with decreased tolerance of effort, and reversible biochemical, hormonal and immunological changes, and an anabolic phase, with a higher adaptive capacity, and enhanced performance. The two main hormonal axes activated in the catabolic phase are sympathetic–adrenal–medullary system and hypothalamic-pituitary-adrenal (HPA) axis, while in the anabolic phase, growth hormone-insulin-like factor I axis, and gonadal axes. The hormonal responses during exercise and recovery can be regarded as regulatory and integrated endocrine responses. The increase of catecholamines and ACTH is dependent on the intensity of exercise; a marked increase in plasma A occurs during exercises with high emotional content. The response of cortisol is correlated with the duration of exercise, while the effect of exercise duration on β-endorphin changes is highly dependent on the type of exercise performed. Cortisol and β-endorphin changes usually occur in phase, but not during exercises with high emotional content. Glucocorticoids and iodothyronines are involved in meeting immediate energy demands, and a model of functional interactions between HPA axis and hypothalamic-pituitary-thyroid axis during exercise stress is proposed. A modulation of coping responses to different energy demanding physical activities required for sport activities could be hypothesized. This review supports the proposed regulation of hypophysiotropic TRHergic neurons as metabolic integrators during exercise stress. Many hormonal systems (ghrelin, leptin, glucose, insulin, and cortisol) are activated to control substrate mobilizations and utilization. The cardiovascular homeostasis, the fluid and electrolyte balance during exercise are highly dependent on vasoactive hormones (antidiuretic hormone, atrial natriuretic peptide, renin–angiotensin–aldosterone, and prostaglandins) control.

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Dissertations / Theses on the topic "Angiotensins. Hormones"

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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 Marcondes
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-26T14:51:39Z (GMT). No. of bitstreams: 1 Costa_Rafaela_D.pdf: 1664351 bytes, checksum: 856190c69c5300d3e8c63ffa3c136ddf (MD5) Previous issue date: 2014
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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Books on the topic "Angiotensins. Hormones"

1

International Symposium on Cellular and Molecular Biology of the Adrenal Cortex (5th 1992 Avignon, France). Cellular and molelcular biology of the adrenal cortex: Proceedings of the 5th International Symposium on Cellular and Molecular Biology of the Adrenal Cortex held in Avignon (France) August 27-29, 1992. Paris, France: INSERM, 1992.

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Kidney Hormones: Erythropoietin (Kidney Hormones). Academic Press, 1997.

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Fisher, J. W. Kidney Hormones. Academic Press, 1986.

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(Editor), J. M. Saez, and et al (Editor), eds. Cellular and Molecular Biology of the Adrenal Cortex (Colloques Inserm). John Libbey & Co Ltd, 1992.

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Cellular and Molecular Biology of the Adrenal Cortex (Colloques INSERM). J. Libbey Eurotext, 1996.

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K, Raizada Mohan, Phillips M. Ian, Sumners Colin, and International Symposium on the Cellular and Molecular Aspects of Angiotensin Receptors (1st : 1994 : Gainsville, Fla.), eds. Recent advances in cellular and molecular aspects of angiotensin receptors. New York: Plenum Press, 1996.

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R, Ruffolo Robert, ed. Angiotensin II receptors. Boca Raton: CRC Press, 1994.

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Ghazi, Nooshin. Variations in AII release from the rat brain during the estrous cycle. 1994.

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Grove, Kevin Lyle. Angiotensin II receptors in the hypothalamus of the adult and developing female rat brain. 1994.

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Vitamin Biosynthesis (Vitamins and Hormones, Volume 60) (Vitamins and Hormones). Academic Press, 2000.

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Book chapters on the topic "Angiotensins. Hormones"

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Corvol, Pierre, Joël Ménard, and Anthony R. Means. "The Renin-Angiotensin-Aldosterone System and Atrial Natriuretic Factor." In Hormones, 595–634. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-3060-8_13.

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Sumners, Collin, and Melvin J. Fregly. "Receptors for Angiotensin II." In Peptide Hormone Receptors, edited by M. Y. Kalimi and J. R. Hubbard, 663–714. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110850246-015.

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Jenkins, T. A., F. A. O. Mendelsohn, A. L. Albiston, and S. Y. Chai. "Angiotensin IV Binding Site." In Hypertension and Hormone Mechanisms, 61–74. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59259-987-5_4.

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Touyz, Rhian M., and Ernesto L. Schiffrin. "Angiotensin II and Inflammation." In Hypertension and Hormone Mechanisms, 91–110. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59259-987-5_6.

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Prieto-Carrasquero, Minolfa C., Hiroyuki Kobori, and L. Gabriel Navar. "The Intrarenal Renin-Angiotensin System." In Hypertension and Hormone Mechanisms, 3–22. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59259-987-5_1.

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Ferrario, Carlos M., David B. Averill, K. Bridget Brosnihan, Mark C. Chappell, Debra I. Diz, Patricia E. Gallagher, Liomar Neves, and E. Ann Tallant. "Regulation of Cardiovascular Control Mechanisms by Angiotensin-(1–7) and Angiotensin-Converting Enzyme 2." In Hypertension and Hormone Mechanisms, 43–59. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59259-987-5_3.

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Kumar, Rajesh, Kenneth M. Baker, and Jing Pan. "Cardiac and Vascular Renin-Angiotensin Systems." In Hypertension and Hormone Mechanisms, 23–42. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59259-987-5_2.

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Re, Richard N. "Intracellular Angiotensin and the Actions of Intracrine Hormones." In Renin Angiotensin System and the Heart, 179–92. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470032103.ch12.

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Carey, Robert M., and Helmy M. Siragy. "Angiotensin AT2 Receptors in Blood Pressure Regulation." In Hypertension and Hormone Mechanisms, 75–89. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59259-987-5_5.

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Novo, S., L. Adamo, A. Giamporcaro, G. Forte, B. Longo, V. Bruno Gallo, G. Licata, and A. Strano. "Changes of Angiotensin Converting Enzyme (Ace) Levels During Activation of the Renin-Angiotensin-Aldosterone System (RAAs)." In Vasodepressor Hormones in Hypertension: Prostaglandins and Kallikrein-Kinins, 339–47. Basel: Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9299-5_35.

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Conference papers on the topic "Angiotensins. Hormones"

1

Westwood, Brian M., Hossam A. Shaltout, and Mark C. Chappell. "Modeling of Angiotensin Peptide Metabolism in Renal Proximal Tubules." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-190990.

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The recent discovery of angiotensin converting enzyme 2 (ACE2) as a functional peptidase within the renin-angiotensin system (RAS) has added a new layer of complexity to the enzymatic cascade of this hormonal system. ACE2 is highly expressed in the proximal tubules of the kidney, an important tissue site involved in blood pressure regulation. Therefore, we derived a model for the processing of Ang I which is the immediate precursor to the biologically active peptides Ang II and Ang-(1-7) based on metabolism data in isolated proximal tubules of the sheep kidney (1). Given the individual experimental velocities for several peptidases expressed in the proximal tubules including ACE, ACE2 and neprilysin, rate constants were calculated to describe the conservation equations for the processing of Ang I, Ang II and Ang-(1-7) We modeled the system with Ang I as the initial substrate and peptide concentrations for the downstream products were calculated using Euler’s method.

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Garcia-Espinosa, Maria A., Glenn J. Lesser, Waldemar Debinski, E. Ann Tallant, and Patricia E. Gallagher. "Abstract 1938: Angiotensin-(1-7), a peptide hormone with therapeutic potential for the treatment of glioblastomas." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1938.

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Petty, William Jeffrey, Antonius A. Miller, Thomas P. McCoy, Patricia E. Gallagher, E. Ann Tallant, and Frank M. Torti. "Abstract B208: Phase I study of angiotensin‐(1–7), an endogenous antiangiogenic hormone: Clinical, pharmacokinetic, and biomarker findings." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b208.

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Cook, KL, D. Soto Pantoja, P. Gallagher, and E. Tallant. "Angiotensin-(1-7) inhibition of human breast tumors with distinct hormone receptor expression results in a differential regulation of Akt." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-3127.

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D'Amora, Paulo, Samuel Marcos Ribeiro de Noronha, Cheryl Alecrim, Marcia Batista Salzgeber, Suma Imura Shimuta, Clovis Ryuichi Nakaie, Afonso Celso Pinto Nazário, Ismael Dale Cotrim Guerreiro da Silva, and Silvana Aparecida Alves Correa-Noronha. "Abstract 266: Angiotensin I-7 modulates transcriptional (de)activation of multiple members of steroid hormone receptor superfamily: Possible mechanisms underlying inhibited proliferation in (T47D) human breast cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-266.

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