Relevant bibliographies by topics / Ouabaina

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  2. Dissertations / Theses
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Academic literature on the topic 'Ouabaina'

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Published: 4 June 2021
Last updated: 27 April 2022

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Journal articles on the topic "Ouabaina"

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Fu, Yong, Dalian Ding, Lei Wei, Haiyan Jiang, and Richard Salvi. "Ouabain-Induced Apoptosis in Cochlear Hair Cells and Spiral Ganglion NeuronsIn Vitro." BioMed Research International 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/628064.

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Ouabain is a common tool to explore the pathophysiological changes in adult mammalian cochleain vivo. In prior studies, locally administering ouabain via round window membrane demonstrated that the ototoxic effects of ouabainin vivovaried among mammalian species. Little is known about the ototoxic effectsin vitro. Thus, we prepared cochlear organotypic cultures from postnatal day-3 rats and treated these cultures with ouabain at 50, 500, and 1000 μM for different time to elucidate the ototoxic effects of ouabainin vitroand to provide insights that could explain the comparative ototoxic effects of ouabainin vivo. Degeneration of cochlear hair cells and spiral ganglion neurons was evaluated by hair-cell staining and neurofilament labeling, respectively. Annexin V staining was used to detect apoptotic cells. A quantitative RT-PCR apoptosis-focused gene array determined changes in apoptosis-related genes. The results showed that ouabain-induced damagein vitrowas dose and time dependent. 500 μM ouabain and 1000 μM ouabain were destructively traumatic to both spiral ganglion neurons and cochlear hair cells in an apoptotic signal-dependent pathway. The major apoptotic pathways in ouabain-induced spiral ganglion neuron apoptosis culminated in the stimulation of the p53 pathway and triggering of apoptosis by a network of proapoptotic signaling pathways.
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Curras, M. C., and J. A. Boulant. "Effects of ouabain on neuronal thermosensitivity in hypothalamic tissue slices." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 1 (July 1, 1989): R21—R28. http://dx.doi.org/10.1152/ajpregu.1989.257.1.r21.

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To determine the role of the electrogenic Na+-K+ pump in neuronal thermosensitivity, single-unit activity was recorded in rat hypothalamic tissue slices before, during, and after perfusions containing 10(-5) or 10(-6) M ouabain, a specific pump inhibitor. Most neurons were recorded in the preoptic-anterior hypothalamus. Some neurons were also tested with high magnesium-low calcium perfusions to determine ouabain's effects on neuronal activity during synaptic blockade. When the neurons were characterized according to thermosensitivity, 24% were warm sensitive, 8% were cold sensitive, and 68% were temperature insensitive. Ouabain increased the firing rate of 60% of all neurons. Ouabain did not reduce the thermosensitivity of cold-sensitive and warm-sensitive neurons; however, temperature-insensitive neurons became more warm sensitive during ouabain perfusion. This increase in warm sensitivity did not occur with ouabain plus high Mg2+-low Ca2+ perfusion, suggesting that Ca2+ is important in this response. These results indicate that the Na-K pump is not responsible for the thermosensitivity of hypothalamic cold-sensitive or warm-sensitive neurons; however, this pump may be actively employed by many neurons that remain insensitive to temperature changes.
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Blanco, Gustavo, and Darren P. Wallace. "Novel role of ouabain as a cystogenic factor in autosomal dominant polycystic kidney disease." American Journal of Physiology-Renal Physiology 305, no. 6 (September 15, 2013): F797—F812. http://dx.doi.org/10.1152/ajprenal.00248.2013.

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The classic role of the Na-K-ATPase is that of a primary active transporter that utilizes cell energy to establish and maintain transmembrane Na+ and K+ gradients to preserve cell osmotic stability, support cell excitability, and drive secondary active transport. Recent studies have revealed that Na-K-ATPase located within cholesterol-containing lipid rafts serves as a receptor for cardiotonic steroids, including ouabain. Traditionally, ouabain was viewed as a toxin produced only in plants, and it was used in relatively high concentrations to experimentally block the pumping action of the Na-K-ATPase. However, the new and unexpected role of the Na-K-ATPase as a signal transducer revealed a novel facet for ouabain in the regulation of a myriad of cell functions, including cell proliferation, hypertrophy, apoptosis, mobility, and metabolism. The seminal discovery that ouabain is endogenously produced in mammals and circulates in plasma has fueled the interest in this endogenous molecule as a potentially important hormone in normal physiology and disease. In this article, we review the role of the Na-K-ATPase as an ion transporter in the kidney, the experimental evidence for ouabain as a circulating hormone, the function of the Na-K-ATPase as a signal transducer that mediates ouabain's effects, and novel results for ouabain-induced Na-K-ATPase signaling in cystogenesis of autosomal dominant polycystic kidney disease.
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McLaughlin, Charles W., Sylvia Zellhuber-McMillan, Anthony D. C. Macknight, and Mortimer M. Civan. "Electron microprobe analysis of rabbit ciliary epithelium indicates enhanced secretion posteriorly and enhanced absorption anteriorly." American Journal of Physiology-Cell Physiology 293, no. 5 (November 2007): C1455—C1466. http://dx.doi.org/10.1152/ajpcell.00205.2007.

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The rate of aqueous humor formation sequentially across the pigmented (PE) and nonpigmented (NPE) ciliary epithelial cell layers may not be uniform over the epithelial surface. Because of the tissue's small size and complex geometry, this possibility cannot be readily tested by conventional techniques. Rabbit iris-ciliary bodies were divided, incubated, quick-frozen, cryosectioned, and freeze-dried for electron probe X-ray microanalysis of the elemental contents of the PE and NPE cells. We confirmed that preincubation with ouabain to block Na+,K+-ATPase increases Na+ and decreases K+ contents far more anteriorly than posteriorly. The anterior and posterior regions were the iridial portion of the primary ciliary processes and the pars plicata, respectively. Following interruption of gap junctions with heptanol, ouabain produced smaller changes in anterior PE cells, possibly reflecting higher Na+ or K+ permeability of anterior NPE cells. Inhibiting Na+ entry selectively with amiloride, benzamil, or dimethylamiloride reduced anterior effects of ouabain by ∼50%. Regional dependence of net secretion was also assessed with hypotonic stress, which stimulates ciliary epithelial cell regulatory volume decrease (RVD) and net Cl− secretion. In contrast to ouabain's actions, the RVD was far more marked posteriorly than anteriorly. These results suggest that 1) enhanced Na+ reabsorption anteriorly, likely through Na+ channels and Na+/H+ exchange, mediates the regional dependence of ouabain's actions; and 2) secretion may proceed primarily posteriorly, with secondary processing and reabsorption anteriorly. Stimulation of anterior reabsorption might provide a novel strategy for reducing net secretion.
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Lewis, Lynley K., Timothy G. Yandle, Philip J. Hilton, Berit P. Jensen, Evan J. Begg, and M. Gary Nicholls. "Endogenous Ouabain Is Not Ouabain." Hypertension 64, no. 4 (October 2014): 680–83. http://dx.doi.org/10.1161/hypertensionaha.114.03919.

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Donaldson, S. K. "Peeled mammalian skeletal muscle fibers. Possible stimulation of Ca2+ release via a transverse tubule-sarcoplasmic reticulum mechanism." Journal of General Physiology 86, no. 4 (October 1, 1985): 501–25. http://dx.doi.org/10.1085/jgp.86.4.501.

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Single muscle fibers from rabbit soleus and adductor magnus and from semitendinosus muscles were peeled to remove the sarcolemma and then stimulated to release Ca2+ by (a) caffeine application or (b) ionic depolarization accomplished via substitution of choline chloride for potassium propionate at constant [K+] X [Cl-] in the bathing solution. Each stimulus, ionic or caffeine, elicited an isometric tension transient that appeared to be due to Ca2+ released from the sarcoplasmic reticulum (SR). The peak magnitude of the ionic (Cl- -induced) tension transient increased with increasing Cl- concentration. The application of ouabain to fibers after peeling had no effect on either type of tension transient. However, soaking the fibers in a ouabain solution before peeling blocked the Cl- -induced but not the caffeine-induced tension transient, which suggests that ouabain's site of action is extracellular, perhaps inside transverse tubules (TTs). Treating the peeled fibers with saponin, which should disrupt TTs to a greater extent than SR membrane, greatly reduced or eliminated the Cl- -induced tension transient without significantly altering the caffeine-induced tension transient. These results suggest that the Cl- -induced tension transient is elicited via stimulation of sealed, polarized TTs rather than via ionic depolarization of the SR.
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Gomez-Sanchez, Elise P., Mark F. Foecking, Deborah Sellers, Mary S. Blankenship, and Celso E. Gomez-Sanchez. "Is the Circulating Ouabain-like Compound Ouabain?" American Journal of Hypertension 7, no. 7_Pt_1 (July 1994): 637–46. http://dx.doi.org/10.1093/ajh/7.7.637.

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Gomez-Sanchez, Elise P., Mark F. Foecking, Sellers Deborah, Mary S. Blankenship, and Celso E. Gomez-Sanchez. "Is the Circulating Ouabain-like Compound Ouabain?" American Journal of Hypertension 7, no. 7_Pt_1 (July 1994): 647–50. http://dx.doi.org/10.1093/ajh/7.7.647.

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Murrell, Julie R., Jeffrey D. Randall, James Rosoff, Ji-liang Zhao, Roderick V. Jensen, Steven R. Gullans, and Garner T. Haupert. "Endogenous Ouabain." Circulation 112, no. 9 (August 30, 2005): 1301–8. http://dx.doi.org/10.1161/circulationaha.105.554071.

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Hamlyn, John M., and Mordecai P. Blaustein. "Endogenous Ouabain." Hypertension 68, no. 3 (September 2016): 526–32. http://dx.doi.org/10.1161/hypertensionaha.116.06599.

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Dissertations / Theses on the topic "Ouabaina"

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Pace, Iuri Domingues Della. "Efeito do Triterpeno 3β, 6β, 16β , trihidroxilup-20(29)-eno nas convul-sões induzidas por pentilenotretazol: papel da Na+, K+ ATPase." Universidade Federal de Santa Maria, 2013. http://repositorio.ufsm.br/handle/1/8993.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Epilepsy is a syndrome characterized by spontaneous recurrent seizures, result of paroxys-mal discharges , excessive or synchronous a neural population . Despite the good prognosis, the high number of patients with epilepsy who have seizures refractory to medication, reflects the lack of a bet-ter understanding of excitotoxic disorders characteristic of this disease. Thus, it becomes important to understand the mechanisms for induction and maintenance of seizures as well, the search for new antiepileptic compounds that may prevent the development of this pathology. As nociception and epi-lepsy have mechanisms in common and several anticonvulsant drugs are used in treatment of pain , we investigated the effect of triterpene 3β , 6β , 16β Trihidroxilup -20 ( 29) -ene (TTHL), a compound with antinociceptive properties in convulsions induced by pentylenetetrazol (PTZ). The TTHL admin-istration ( 30 mg / kg , po) increased the latency to the first myoclonic seizures and tonic- clonic sei-zure and decreased the duration of generalized seizures induced by PTZ . In addition , the administra-tion of TTHL reduced lipid peroxidation and protein carbonylation , as well as protected from inhibition of glutamate uptake and activity of the Na+, K+-ATPase (α1and α2/α3 subunits ) caused by PTZ . Alt-hough the TTHL showed no antioxidant activity per se and not alter the binding of [ 3H ] flunitrazepam to the site of the GABAA receptor bezodiazepínico , this protected compound of convulsions and inhi-bition of Na+, K+-ATPase activity induced by ouabain . These results suggest that the anticonvulsant action is due TTHL s maintenance of Na+, K+-ATPase . In fact , the experiments performed in the cer-ebral cortex in vitro showed that PTZ ( 10 mM ) reduced the activity of Na+, K+-ATPase and that prein-cubation with TTHL ( 10 mM ) protected from this inhibition.Thus , these data indicate that the protec-tion exerted by TTHL this seizure model is not related to antioxidant activity or GABAergic activity . However, these results demonstrate that effective protection of Na+, K+-ATPase activity induced by this compound protects against oxidative and excitotoxic damage induced by PTZ .
A epilepsia é uma síndrome caracterizada por crises espontâneas e recorrentes, resultado de descargas paroxísticas, excessivas e sincrônicas de uma população neural. Apesar do bom prognós-tico, o elevado número de pacientes com epilepsia, que apresentam convulsões refratárias aos medi-camentos, reflete a falta de um melhor entendimento dos distúrbios excitotóxicos característico desta doença. Desta forma, torna-se importante o entendimento dos mecanismos de indução e manuten-ção das convulsões, bem como, a busca por novos compostos anticonvulsivantes que possam evitar o desenvolvimento desta patologia. Como a nocicepção e a epilepsia possuem mecanismos em co-mum, e vários anticonvulsivantes são usados no tratamento da dor, foi investigado o efeito do Triter-peno 3β,6β,16β Trihidroxilup-20(29)-eno (TTHL), um composto com propriedades antinociceptivas, nas convulsões induzidas pelo pentilenotetrazol (PTZ). A administração do TTHL (30 mg/kg; p.o) au-mentou a latência para a primeira convulsão mioclônica e tônico-clônica e reduziu a duração das convulsões generalizadas induzidas pelo PTZ. Além disso, a administração do TTHL reduziu a pero-xidação lipídica e a carbonilação de proteínas, assim como, protegeu da inibição da captação de glu-tamato e da atividade da Na+,K+-ATPase (subunidades α1 e α2/α3) causadas pelo PTZ. Embora, o TTHL não mostrou uma atividade antioxidante per se e não alterou a ligação do [3H]flunitrazepam ao sítio para bezodiazepínico do receptor GABAA, este composto protegeu das convulsões e da inibição da atividade da Na+, K+- ATPase induzidos pela ouabaina. Estes resultados sugerem que a ação an-ticonvulsivante do TTHL é devido s manutenção da atividade da Na+,K+-ATPase. De fato, os experi-mentos realizados no córtex cerebral in vitro mostraram que o PTZ (10 mM) reduziu a atividade da Na+,K+-ATPase e que a incubação prévia com TTHL (10 μM) protegeu desta inibição. Dessa forma, estes dados indicam que a proteção exercida pela TTHL neste modelo de convulsão não está relaci-onado com atividade antioxidante ou a atividade GABAérgica. No entanto, estes resultados demons-traram que a proteção eficaz da atividade da Na+,K+-ATPase , induzida por este composto, protege contra os danos excitotóxic e oxidativos induzidos pelo PTZ.
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Carneiro, Luciana Teles. "Efeito modulador da ouabaína no sistema imunológico." Universidade Federal da Paraí­ba, 2011. http://tede.biblioteca.ufpb.br:8080/handle/tede/6866.

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Initially known as a cardiotonic steroid capable to inhibit the Na+/K+ATPase, ouabain was identified as an endogenous substance present in human plasma, produced by the adrenal, pituitary and hypothalamus and can interfere with various aspects of immune response. In this study, which aimed to study the modulating effect of ouabain on the immune system in vivo and in vitro using mouse models, we demonstrated that treatment for three consecutive days using 0,56 mg/kg ouabain was able to reduce cell migration induced by mitogen Concanavalian A (Con A) to the peritoneum, and this fact reflects a decrease in the number of polymorphonuclear leukocytes, mainly neutrophils. In this same model, ouabain was also able to increase the number of mononuclear leukocytes in the peritoneal cavity. Evaluating the effect of treatment on lymphocytes in peripheral organs, we found that, in lymphocytes from mesenteric lymph nodes, this substance induces a decrease of 20% of T CD3+ lymphocytes, concomitant with an increase in same percentage of B lymphocytes, without, however, modulating the proportion of CD4+ and CD8+ among themselves, as well as the number of regulatory T cells (CD4+/CD25+). In the thymus, the same treatment, does not affect the proportion of lymphocyte subpopulations studied. The analysis qualitative and quantitatively of peripheral blood leukocytes, biometrics and cellularity of spleen, thymus and lymph nodes showed no change in response to ouabain treatment. Comparative studies using treatment for one or two days, with the same dose of 0,56 mg/kg did not trigger modulation, in vivo, in populations of T lymphocytes, B lymphocytes and subpopulations of CD4+ and CD8+ cells in mesenteric lymph nodes. In addition, ouabain was able to inhibit mitochondrial activity of lymphocytes stimulated with Con A, using MTT assay.These findings indicate an immunomodulatory role of ouabain.
Inicialmente, conhecida como um esteróide cardiotônico e por sua propriedade de inibir a Na+/K+ATPase, a ouabaína foi identificada como uma substância endógena presente no plasma humano, produzida pela adrenal, hipófise e hipotálamo e capaz de interferir em vários aspectos da resposta imune. Neste trabalho, que teve como objetivo estudar o efeito modulador da ouabaína no sistema imunológico in vivo e in vitro por meio de modelos murinos, demonstrou-se que o tratamento por três dias consecutivos com ouabaína utilizando a dose de 0,56 mg/kg foi capaz de reduzir a migração celular induzida pelo mitógeno Concanavaliana A (Con A) para o peritôneo, sendo este fato reflexo da redução do número de leucócitos polimorfonucleares, principalmente, neutrófilos. Neste mesmo modelo, a ouabaína também foi capaz de aumentar o número de leucócitos mononucleares no lavado peritoneal. Avaliando-se o efeito desse tratamento no perfil linfocitário de órgãos periféricos, encontrou-se que, em linfócitos de linfonodos mesentéricos, esta substância induz a uma diminuição de 20% de linfócitos T CD3+, concomitante a um aumento de mesmo percentual de linfócitos B, sem, no entanto, modular a proporção de linfócitos TCD4+ e CD8+ entre si, bem como o número de células T regulatórias (CD4+CD25+). No timo, o mesmo tratamento com a ouabaína não interfere na proporção das subpopulações linfocitárias estudadas. As análises qualitativas e quantitativas de leucócitos do sangue periférico, da biometria e celularidade do baço, timo e linfonodos mesentéricos não apresentaram alteração em resposta ao tratamento com a ouabaína. Estudos comparativos utilizando tratamentos de um ou dois dias, com a mesma dose de 0,56 mg/Kg não desencadearam modulação, in vivo, nas populações de linfócitos T, linfócitos B e das subpopulações de linfócitos TCD4+ e CD8+ nos linfonodos mesentéricos. Adicionalmente, a ouabaína foi capaz de inibir a atividade mitocondrial de linfócitos estimulados com Con A, por meio do ensaio de MTT. Estes resultados indicam um papel imunomodulador da ouabaína.
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Vasconcelos, Danielle Ingrid Bezerra de. "Análise do efeito imunomodulador da ouabaína na inflamação e nocicepção." Universidade Federal da Paraí­ba, 2011. http://tede.biblioteca.ufpb.br:8080/handle/tede/3640.

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Ouabain, known as a cardiotonic glycoside capable of inhibiting the Na+/K+ ATPase, was widely used for heart failure treatment. Identified as an endogenous substance, ouabain is capable of interfering with various physiological functions, including immune system modulation. Besides that, little is known about the involvement of this substance in nociceptive and inflammatory processes. The present study investigated the role of ouabain in acute peripheral inflammation induced by intraplantar administrartion of different phlogistic agents (carrageenan, compound 48/80, histamine, bradykinin, and PGE2) and in nociceptive processes (abdominal writhing induced by acetic acid and hot plate). Ouabain produced a significant reduction in the mouse paw edema induced by carrageenan and compound 48/80. This antiinflammatory effect of ouabain is associated to the inhibition of PGE2, bradykinin, and mast-cell degranulation, but not to histamine. Ouabain also presented a central and peripheral anti-nociceptive activity. This analgesic potential might be related to the inhibition of inflammatory mediators and to activation of opioid receptors, since it was reversed by naloxone, an opioid antagonist. Additionally, the analgesic effect of ouabain was not related to sedative effect or to motor function. Taken together, the present work demonstrated for the first time, in vivo, the antiinflammatory and analgesic potential of ouabain
A Ouabaína é um glicosídeo cardiotônico, inibidor da Na+/K+-ATPase, utilizada na clínica para o tratamento de insuficiência cardíaca. Atualmente, sabe-se que essa substância é endógena, e capaz de interferir em várias funções fisiológicas, inclusive em diversos aspectos do sistema imunológico. Apesar disso, pouco se sabe sobre seu envolvimento em processos inflamatórios e nociceptivos. Neste trabalho, foi avaliada a atividade da Ouabaína na inflamação aguda desencadeada pela administração de diversos agentes flogísticos (carragenina, composto 48/80, histamina, PGE2 e bradicinina) e em modelos nociceptivos (contorções abdominais induzidas por ácido acético e placa quente). A Ouabaína produziu uma redução no edema de pata produzido por carragenina e pelo composto 48/80. Esse potencial anti-inflamatório está relacionado ao bloqueio da degranulação de mastócitos, bem como pela inibição da via da PGE2 e da bradicinina, porém é independente da via da histamina. A Ouabaína também apresentou uma atividade anti-nociceptiva central e periférica. Esse efeito está vinculado à inibição da via dos mediadores inflamatórios e a mecanismos opióides, visto que foi revertido pela administração da naloxona, um inibidor dos receptores opióides. Adicionalmente, foi descrito que a inibição da dor pela Ouabaína não possui envolvimento com sedação ou diminuição da capacidade motora. O conjunto desses dados demonstra pela primeira vez, in vivo, a atividade anti-inflamatória e anti-nociceptiva da Ouabaína.
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Kinoshita, Paula Fernanda. "Sinalização inflamatória e a modulação da expressão de genes induzida pela ação da ouabaína nas isoformas a1, a2 - Na+, K+- ATPase em células da glia." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-24052014-103350/.

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Na,K-ATPase é uma proteína de membrana que tem como função manter o equilíbrio osmótico nas células pela hidrólise de ATP. A ouabaína (OUA) se liga a Na,K-ATPase e é capaz de ativar cascatas de sinalização. As subunidades a da Na,K-ATPase possuem 4 isoformas que são distribuídas de forma diferenciada nos tecidos. As células da glia são importantes na resposta contra lesões no cérebro e também controlam a inflamação. Dados na literatura mostram que a OUA tem efeito protetor em alguns tipos de dano. O objetivo do estudo é avaliar a função da isoforma a2 na cultura de células da glia em resposta à OUA e ao LPS. Nós investigamos a ação da OUA em diversas concentrações e LPS (1g/mL) na viabilidade celular (LDH) e proliferação celular (MTT). O LPS foi utilizado como modelo de inflamação e uma das perguntas era se o tratamento prévio com OUA, seria capaz de reverter a ativação do fator de transcrição NF-kB que está envolvido com inflamação. O pré-tratamento com OUA diminuiu a ativação do NF-kB induzida pelo LPS. Após, nós silenciamos a isoforma a2 das células da glia com RNAi. Os nossos dados mostram que o pré-tratamento com OUA reverte o efeito na ativação do NF-kB causado pelo LPS. Provavelmente, a isoforma a2 está relacionada com alguma via de sinalização que interage com a via do LPS.
Na,K-ATPase is a conserved membrane protein which maintains the osmotic balance in the cell by the hydrolysis of ATP. Ouabain (OUA) binds to Na,K-ATPase and it can activate signaling pathways. The a subunits of Na,K-ATPase have 4 isoforms which are distributed in a different pattern in the tissues. Glial cells have an important role in the response against injury and they also control inflammation. Some data have reported that OUA can protect against some types of injury. The aim of this study is to evaluate the role of a2 isoform in glial cells in response to OUA and LPS stimulus. We investigated the action of OUA and LPS in cell viability (LDH) and cell proliferation (MTT). LPS was used as a model of inflammation and one of our questions was if the treatment with OUA before LPS was capable of reduce the activation of the transcription factor NF-kB which is involved in inflammation. The pre-treatment with OUA decreased the NF-kB activation induced by LPS. We also silenced the a2 isoform in culture glial cells with iRNA. Taken together our data showed that OUA pretreatment reversed the NF-kB activation induced by LPS in primary cultures of glial cells from mice. Probably,the a2 isoform is related with some signaling pathway that interacts with the LPS pathway.
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Cellnik, Torsten [Verfasser]. "Defunktionalisierung von Ouabain / Torsten Cellnik." Wuppertal : Universitätsbibliothek Wuppertal, 2019. http://d-nb.info/118842209X/34.

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Neto, Hildebrando Candido Ferreira. "Papel dos rins na hipertensão arterial induzida pelo tratamento crônico com ouabaína em ratos." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-02022010-105527/.

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A Na+K+-ATPase (NKA) é uma proteína de membrana que participa de mecanismos de transporte nos túbulos renais para a reabsorção de sódio e outros substratos. Sabe-se que a administração de ouabaína (OUA), um inibidor da NKA, induz hipertensão arterial em ratos. No entanto, o papel dos rins nesse modelo de hipertensão não está bem elucidado. Desta forma, o objetivo do presente estudo foi avaliar as possíveis alterações na função renal induzidas pelo tratamento crônico com OUA por 5 ou 20 semanas. Sendo assim, foi observado que o tratamento com OUA promoveu hipertensão de mesma magnitude nos dois grupos avaliados. Além disso, a administração de OUA induziu o aumento da ingestão de água, do fluxo urinário e da expressão protéica da isoforma 1 da NKA. Porém, não foi capaz de alterar de maneira significativa o ritmo de filtração glomerular, assim como a fração de excreção de Na+ e K+. Pode-se concluir que, o tratamento crônico com OUA induz hipertensão, porém parece que os rins não contribuem de forma importante para o processo hipertensivo neste modelo de hipertensão.
Na+K+-ATPase (NKA) is an integral membrane protein that participates in transport mechanisms along renal tubules for sodium reabsorption and other substrates. Its known that ouabain (OUA) administration, a NKA inhibitor, induces hypertension in Wistar rats. However, the role of kidneys in this model of hypertension is not elucidated. So, the aim of this study was to evaluate the possibles alterations in renal function induced by chronic treatment with OUA by 5 or 20 weeks. Chronic treatment with OUA induced hypertension in a similar magnitude in both experimental groups. Moreover, OUA administration was able to increase water intake, urinary flow, and protein expression of 1 isoform of NKA. However, OUA treatment did not alter significantly the glomerular filtration rate, likewise the fractional excretion of Na+ and K+. In summary, chronic OUA treatment induces mild hypertension independent of the period of administration, but the kidneys dont play an important role in the hypertensive process in this model of hypertension.
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Orellana, Ana Maria Marques. "Administração intrahipocampal de Ouabaína ativa o NF - kB e a sinalização da proteína WNTem ratos." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-25052012-083840/.

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A enzima Na+, K+-ATPase é uma proteína de membrana altamente conservada em eucariotos, capaz de gerar um gradiente eletroquímico, fundamental para o balanço osmótico das células, o potencial de repouso das membranas e a propriedade excitatória das células musculares e nervosas. Além de seu papel regulatório na homeostasia iônica, desempenha um papel na transdução de sinal e na ativação de transcrição gênica, modulando na presença de ouabaína o crescimento celular, migração e morte celular programada. A Ouabaína (OUA) é um esteróide cardiotônico, produzido no córtex da adrenal e no hipotálamo. Em linhas gerais, a sinalização da Na+, K+-ATPase promovida pela OUA parece ativar vias associadas à modulação de fatores de transcrição como a via da Src, MAPK, Ca2+ e NF-kB. Evidências indicam que o NF-kB exerça algum tipo de modulação na via canônica do WNT, no entanto os mecanismos moleculares ainda são desconhecidos. A via de sinalização WNT desempenha função importante na embriogênese e na homeostase de tecidos adultos. Assim, o objetivo do presente projeto é verificar se a administração intrahipocampal de OUA é capaz de modular a atividade das vias canônicas do NF-kB e da WNT. Estas vias foram estudadas em um decurso temporal imediato (1 -2 horas) e tardio (10, 24 e 48 horas) utilizando técnicas como Western Blotting, RT-PCR e EMSA. Os resultados encontrados mostram que a OUA (10 nM) foi capaz de ativar a via de sinalização NF-kB, após 1 hora, 10, 24 e 48 horas. A OUA também foi capaz de ativar a via canônica do WNT, sendo que após 10 horas ocorreu aumento da proteína pGSK-3b, enquanto que em 24 horas, observamos aumento da translocação nuclear da b-CATENINA. Além disso, pode-se verificar aumento de BDNF ao longo de todo o decurso temporal.
The enzyme Na+,K+-ATPase is an integral membrane protein, highly conserved in eukaryotes, that establishes the electrochemical gradient across the plasma membrane, which is essential to maintain the osmotic balance of cells, the resting membrane potential and the excitatory property of nerve and muscle cells. Besides its role in ion homeostasis, several recent studies suggest that this pump may also act as a signal transducer and transcription activator involved in cell growth, differentiation and programmed cell death. Ouabain (OUA), the ligand of Na+,K+-ATPase, is a steroid derivative that is produced by the adrenal cortex and hypothalamus. After OUA binding, the Na+,K+-ATPase signaling seems to activate pathways such as Src, MAPK, NF-kB and Ca2+. Some evidences indicate a possible crosstalk between the NF-kB signaling pathway and the canonical WNT pathway, however the molecular mechanisms are still unknown. The canonical WNT play important roles during embryogenesis and in adult tissue homeostasis. The aim of this project is to verify if the intrahipocampal administration of OUA is able to modulate the activity of the canonical pathways of NF-kB and WNT. Both pathways were studied after 1 and 2 hours, and after 10, 24 and 48 hours by methods such Western blot, RT-PCR and Electrophoretic mobility shift assays. The results show that the OUA (10 nM) was able to activate the signaling pathway NF-kB after 1, 10, 24 and 48 hours. The OUA was also able to activate the canonical WNT pathway, since after 10 hours there was an increased in pGSK-3b protein, whereas in 24 hours, we observed increased nuclear translocation of b-CATENIN. Moreover, we found increased levels of BDNF throughout the time course.
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Magnusson, Emma. "Ouabain Toxicity -Selectivity Towards Renal Cancer Cells." Thesis, KTH, Skolan för kemi, bioteknologi och hälsa (CBH), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-278574.

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Ouabain and other cardiotonic steroids are known to inhibit Na + ,K + -ATPase (NKA), theion pump responsible for the ionic gradient across the plasma membrane. These steroidsdisplay a selective toxicity towards several tumour cells in comparison to primary humancells, however, the mechanism behind this is not yet understood. Here, we examined theouabain toxicity in renal epithelial cells, proximal tubular cells (PTCs) of different origin. Weinvestigated the relative cytotoxicity in cancer cells (A-498) and papilloma virus-transformedPTCs (HK-2) as well as to primary human PTCs (hPTC) to validate key components in theeffect. In exposure to ouabain, we examined the cell viability and density by MTT and CrystalViolet assays, and cell migration by a scratch assay. The cytotoxic effect was also studied invarious pH, glucose and potassium ion concentrations. In addition, apoptosis was examinedby the TUNEL assay, and if ouabain kills cancer cells through activation of thevolume-regulated anion channel VRAC channel via NKA. We found that there is a decrease in viable cells when cells are exposed to ouabain ≥ 10nM, however, the effect was not seen to be selective towards cancer cells, nor due toapoptosis and the activation of VRAC. The cytotoxic effect was greater in more acidicextracellular pH ~6.8, but independent of glucose concentration in the medium. Interestingly,the effect was also reversed at an increased extracellular concentration of potassium, andouabain did selectively inhibit the cancer cells to migrate. Thus, there could be potential forouabain to act as an anti-cancer agent for renal cancer and to inhibit tumour metastasization.
Ouabain och andra kardiotoniska steroider är kända för att inhibera Na + ,K + -ATPas (NKA),membranpumpen som är ansvarig för den aktiva jontransporten av natrium och kalium ochjongradienten över plasmamembranet. De har påvisat en selektiv toxicitet mot vissatumörceller i jämförelse med primära humana celler, men det är dock inte förstått hurmekanismen bakom denna företeelse fungerar. I denna studien undersökte vi ouabainstoxicitet i njurcancerceller (A-498) och papillomavirustransformerade proximala tubuliceller(hPTC) för att identifiera effektens nyckelkomponenter. Vid exponering av ouabain undersökte vi cellviabiliteten och -densiteten genom MTT- ochkristallviolett-analyser, samt cellmigrering genom scratch-analys. Den cytotoxiska effektenstuderades också under olika pH-förhållanden samt glukos- och kaliumkoncentrationer.Dessutom undersöktes det om apoptos orsakar celldöd genom TUNEL-analys, och omouabain dödar njurcancerceller genom aktivering av den volymreglerade anjonkanalen(VRAC) via NKA. Vi fann minskning av cellernas livskraft vid exponering av ≥ 10 nM ouabain, men effektentycktes dock inte se ut att vara selektiv gentemot cancerceller, inte heller på grund av apoptosoch aktivering av VRAC. Den cytotoxiska effekten var större vid lägre pH, men oberoendeav mediets glukoskoncentrationen. Intressant nog motverkades också effekten vid förhöjdkoncentration av kaliumjoner, och ouabain hämmade selektivt cancercellerna att migrera.Således finns det en viss potential för ouabain att kunna fungera som ett anticancermedel motnjurcancer och att hämma metastasutveckling.
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Harwood, Steven Michael. "Development and application of an immunoassay for ouabain and a study of the nature of endogenous ouabain-like compound." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325540.

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Leite, Jacqueline Alves. "Atividade imunomoduladora da ouabaína no processo inflamatório agudo." Universidade Federal da Paraí­ba, 2012. http://tede.biblioteca.ufpb.br:8080/handle/tede/6731.

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Ouabain (OUA), a potent inhibitor of the Na+,K+-ATPase pump, was identified as an endogenous substance of human plasma. In recent years, ouabain was shown to affect various immunological processes. Mechanisms that involve cellular differentiation, proliferation, activation and migration, as well as inflammatory mediators release, are activated during inflammation and homeostasis is usually reestablished. This study demonstrated the modulatory ability of OUA on inflammatory process. Aim: This study aimed to evaluate ouabain immunomodulatory role on acute inflammatory process using a murine model. Methods: Initially, a dose and time-response curve was performed with OUA (0.10 mg/kg, 0.31 mg/kg and 0.56 mg/kg) intraperitoneally administered on the paw edema induced by zymosan (10 mg/mL). Mice were also intraperitoneally (i.p.) stimulated with zymosan (2 mg/mL). After 4h, the peritoneal fluid was removed for total and differential cell counts. Neutrophils and macrophages population, as well as cell viability, were analyzed using an annexin KIT by flow cytometry. The concentrations of the cytokines IL-1β, TNF-α, IL-6 and IL-10 in peritoneal lavage fluids were assayed using ELISA kit. Ouabain influence in the vascular permeability increase was determined using evans blue dye. OUA, in vitro, influence on nitric oxide (NO) production was also studied. Results: It was observed that OUA 0,56 mg/kg injected for three consecutive days prevented zymosan edema formation . After induction of inflammation, treatment with OUA led to a 42% reduction in the total cell numbers in the peritoneal cavity, as a reflex of the inhibition of polymorphonuclear leukocytes (54%), which was not due to cell apoptosis. Ouabain also decreased zymosan-induced plasma exudation (33%). Furthermore, OUA decreased the levels of TNF-α (64%) and IL-1β (63%), without interference on IL-6 and IL-10 levels. It was also demonstrated, using peritoneal macrophages, that ouabain did not interfere on LPS induced NO production. Conclusion: Ouabain modulated the acute inflammatory response induced by zymosan. However, further studies are necessary to elucidate the mechanisms involved
A ouabaína (OUA), um potente inibidor da Na+/K+-ATPase, foi identificada como uma substância endógena presente no plasma humano. Nos últimos anos, foi evidenciado que a OUA é capaz de interferir em diversos aspectos do sistema imunológico. Durante o processo inflamatório, são ativados mecanismos que envolvem a diferenciação, proliferação, ativação e migração celular, além da liberação de mediadores inflamatórios, e geralmente, ocorre o retorno à homeostasia. Este trabalho demonstrou a capacidade moduladora da OUA no processo inflamatório. Objetivo: Avaliar o papel imunomodulador da OUA na inflamação aguda em modelo murino. Métodos: Inicialmente, foi realizada uma curva de tempo e dose-resposta com a OUA (0,10 mg/kg; 0,31 mg/kg e 0,56 mg/kg) administrada de forma intra-peritoneal (i.p.) no modelo de edema de pata induzido por zimosan (10mg/mL). Os camundongos também foram estimulados com zimosan i.p.(2mg/ml). Após 4h, o fluido peritoneal foi removido para a contagem total e diferencial das células. Foi realizada a análise das populações de neutrófilos e macrófagos, além da viabilidade celular utilizando o kit anexina por citometria de fluxo. As concentrações das citocinas IL-1β, TNF-α, IL-6 e IL-10 no fluido peritoneal foram testadas por ELISA. Foi determinada a interferência do tratamento com a OUA no aumento da permeabilidade vascular. Também foi estudado, in vitro, o efeito de diferentes concentrações de OUA (10 nM, 100 nM e 1000 nM) na produção de óxido nítrico (NO). Resultados: No modelo do edema de pata, observamos que são necessários três dias consecutivos de tratamento na dose de 0,56 mg/kg para que a atividade anti-inflamatória da OUA seja identificada. No modelo de peritonite induzida por zimosan, o pré-tratamento com a OUA reduziu em 42% no número total de células na cavidade peritoneal, como um reflexo da inibição de leucócitos polimorfonucleares (54%). No entanto, este fenômeno não esta associado a apoptose destas células. A OUA também diminuiu o extravasamento de plasma induzido por zimosan (33%) e reduziu os níveis de TNF-α (64%) e IL-1β (63%), sem alterar os níveis de IL-6 e IL-10. Na cultura de macrófagos peritoneais, a OUA não interferiu na produção de NO. Conclusão: Este conjunto de dados sugere que a OUA possui uma atividade anti-inflamatória. No entanto, mais estudos são necessários para elucidar os mecanismos envolvidos.
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Books on the topic "Ouabaina"

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Dare, Amos O. Ouabain potentiates kainate neurotoxicity: A new rat model of human temporal lobe epilepsy. [New Haven, Conn: s.n.], 1996.

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Book chapters on the topic "Ouabaina"

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Ezzaher, Abdellatif, Renaud Mougenot, Alain Gerbi, Nour el Houda Bouanani, Antoine Baggioni, Bertrand Crozatier, and Jean-Michel Maixent. "Non Effectiveness of Ouabain and Decrease in Na+/K+ -ATPase Affinity for Ouabain in Failing Rabbit Heart." In The Sodium Pump, 828–31. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-72511-1_151.

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Hamlyn, J. M. "Discovery of Endogenous Ouabain — A New Mammalian Hormone." In The Sodium Pump, 722–31. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-72511-1_132.

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Navaratnam, S., and J. C. Khatter. "Protective Effect of Nifedipine upon Ouabain-Induced Arrhythmias." In Developments in Cardiovascular Medicine, 59–73. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2057-9_5.

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Lingrel, Jerry B., James Van Huysse, William O’Brien, Elizabeth Jewell-Motz, and Patrick Schultheis. "Amino Acid Residues Involved in Ouabain Sensitivity and Cation Binding." In Molecular and Cellular Mechanisms of H+ Transport, 173–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79301-1_20.

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Lee, Yee-Ki, Kwong-Man Ng, Wing-Hon Lai, Yau-Chi Chan, Yee-Man Lau, Hung-Fat Tse, and Chung-Wah Siu. "Differentiation of Embryonic Stem Cells into Cardiomyocytes: Role of Ouabain." In Stem Cells and Cancer Stem Cells, Volume 6, 71–78. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2993-3_7.

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Rhee, Hee Min. "Parallelism Between Transport Inhibition and L1210 Cell Growth by Ouabain." In Oxygen Transport to Tissue X, 727–34. New York, NY: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9510-6_89.

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Haimann, C., F. Torri-Tarelli, R. Fesce, and B. Ceccarelli. "Calcium Independent Depletion of Quanta and Synaptic Vesicles Induced by Ouabain." In Topics in the Neurosciences, 535–36. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2307-5_35.

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Stokke, E. S., J. Østensen, and F. Kiil. "Effect of Ouabain and Acetazolamide on Proximal Tubular Transport in Dogs." In Diuretics: Basic, Pharmacological, and Clinical Aspects, 82–84. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2067-8_17.

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Grupp, G., Ingrid L. Grupp, T. Hickerson, S. W. Lee, and A. Schwartz. "Biphasic contractile response to ouabain: Species specific? Calcium dependent? Altered sensitivity?" In Cardiac Glycosides 1785–1985, 99–108. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11292-2_15.

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Petzinger, E., K. Fischer, and H. Fasold. "Role of the bile acid transport system in hepatocellular ouabain uptake." In Cardiac Glycosides 1785–1985, 297–304. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11292-2_40.

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Conference papers on the topic "Ouabaina"

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Krivoi, Igor. "ENDOGENOUS OUABAIN AND SKELETAL MUSCLE." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m446.sudak.ns2019-15/245-246.

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Bikmurzina, Anastasia, Arina Fedorova, Igor Krivoi, and Alexander Markov. "CHANGES IN THE BLOOD-BRAIN BARRIER OF RATS WITH CHRONIC INJECTIONS OF OUABAIN." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m951.sudak.ns2020-16/100.

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Rhee, Chung-Ku, Sung Huyn Bae, So-Young Chang, Phil-Sang Chung, and Jae-Yun Jung. "Effect of low level laser therapy (LLLT) on ouabain induced auditory neuropathy in gerbils (Conference Presentation)." In Optical Imaging, Therapeutics, and Advanced Technology in Head and Neck Surgery and Otolaryngology, edited by Brian J. F. Wong and Justus F. Ilgner. SPIE, 2016. http://dx.doi.org/10.1117/12.2212553.

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Wu, Jun, Mariele Mondala, Meng-Yin Hsieh, Eugene Roberts, and Richard Ermel. "Abstract 4403: Antitumor properties of ouabain in lipid double emulsion integrated with tumor cell membrane fractions." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4403.

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Wu, Jun, Meng-Yin Hsieh, Yan Wang, Eugene Roberts, Derek Vallejo, Abraham Lee, and Richard Ermel. "Abstract 5412: Antitumor properties of ouabain in lipid double emulsion in orthotopic canine osteosarcoma xenografted mouse model." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5412.

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Hwang, Mihwa, Dong Wha Jun, Hyun Jung Kim, Soo Kyung Hwang, Chang-Hun Lee, and Sunshin Kim. "Abstract 3335: Ouabain, a cardiac glycoside, inhibits the Fanconi Anemia-BRCA pathway activated by DNA crosslinking agents." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3335.

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Furihata, Kenichi, Diane J. Nugent, Amy L. Bissonette, Elizabeth Vokac, and Thomas J. Kunicki. "PRODUCTION OF HUMAN MONOCLONAL ANTIBODIESSPECIFIC FOR PLATELET MEMBRANE GLYCOPROTEIN IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643705.

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Human monoclonal antibodies specific for platelet membrane glycoproteins (GPs) arepotentially important reagentsfor studies of the immunogenicity of membrane glycoproteins. A human monoclonalautoantibody, 5E5, reactive with plateletGPIIIa has been developed (Nugent, et al.,Blood, 1987, in press). In this report, we describe the production of additional human monoclonal antibodies specific for GPIIIa. Peripheral blood lymphocytes fromone patient with post-transfusion purpur(PTP) and one woman who had delivered an infant with neonatal alloimmune thrombocytopenic purpura (NATP) were used as a source of antigen-specific lymphocytes. A B-lympho-cyte-enriched population was transformed with Epstein Barr virus, strain B95-8, and cultured in microtiter plates. After two weeks, culture supernatants were screened by an antigen-capture ELISA wherein murine monoclonal antibody specificfor the GPIIb-IIIa complex was used to holdcorresponding antigen from a lysate ofnormal platelets. B-lymphoblastoid cell lines producing IgG and/or IgM antibodies were expanded and either cloned by limiting dilution technqiue or hybridized with a HAT-sensitive, ouabain-resistant heterohybrid fusion line, F6, using polyethylene glycol. Hybridomas were selected in medium containing HAT andouabain. After twoweeks, hybridomas producing anti-GPIIb and/or anti-GPIIIa antibody were cloned by limiting dilution. Culture supernatants from cloned B-lymphoblastoid cell lines and cloned hybridomas were rescreened by ELISA wherein affinity-purified GPIIIa or other platelet GP weredirectly conjugatedto microtiter plates. One IgM antibody produced by acloned B-lymphoblastoid cellline (CH16) andtwo IgG antibodies produced bycloned hybridomas(Del5.19 and Del5.23) were shownto react with GPIIIa but not other GP. Further characterization of these human monoclonal antibodies, produced continuouslyin culture now for four months, is in progress.
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