Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/30367
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dc.contributor.authorSpadari-Bratfisch, Regina C. [UNIFESP]
dc.contributor.authorSantos, Iraides Nunes dos
dc.contributor.authorKvetnansky, R.
dc.contributor.authorAguilera, G.
dc.contributor.authorGoldstein, D.
dc.contributor.authorJezova, D.
dc.contributor.authorKrizanova, O.
dc.contributor.authorSabban, E. L.
dc.contributor.authorPacak, K.
dc.date.accessioned2016-01-24T13:49:28Z-
dc.date.available2016-01-24T13:49:28Z-
dc.date.issued2008-01-01
dc.identifierhttp://dx.doi.org/10.1196/annals.1410.075
dc.identifier.citationStress, Neurotransmitters, and Hormones: Neuroendocrine and Genetic Mechanisms. Oxford: Blackwell Publishing, v. 1148, p. 377-383, 2008.
dc.identifier.issn0077-8923
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/30367-
dc.description.abstractSeveral cardiovascular disorders have been related to alterations in beta-adrenoceptor (beta-AR) signaling at or beyond the receptor level. During the stress reaction, the sympathetic-adrenal medullary system and the hypothalamus-pituitary-adrenal cortex axis are activated, causing beta-AR overstimulation and remodeling of the beta(1)/beta(2)/beta(3)-AR ratio in cardiomyocytes. in a model of foot-shock stress, we described decreased STAR signaling occurring simultaneously with increased beta(2)-AR signaling, whereas the response to the nonconventional agonist, CGP12177, was not altered. These alterations may play an adaptive role to the increased sympathetic drive to the heart, protecting the cardiac tissue from the cardiotoxic effects mediated by beta(1)-ARs overstimulation without altering cardiac output, since this would be sustained by the beta(2)-AR, which would also protect myocytes from apoptosis. Moreover, the selective enhancement of the beta(2)-AR population might help to diminish the risk of overstimulation since this adrenoceptor subtype couples to both, stimulatory G (Gs) and inhibitory G (Gi) proteins. On the other hand, in the model of neurogenic hypertension, the decrease in beta(1)-AR-mediated response is not followed by increase in the beta(2)-AR-mediated response. However, the response to CGP12177, which was desensitized 48 h after the surgery, was normalized 7 days after that, when beta(1)-AR were downregulated. Therefore, both experimental models provided evidence that the classical isoform of beta(1)-AR and the recently described low-affinity isoform of beta(1)-AR show independent behavior and provide the heart with adaptive mechanisms to increased sympathetic stimulation during stress.en
dc.format.extent377-383
dc.language.isoeng
dc.publisherBlackwell Publishing
dc.relation.ispartofStress, Neurotransmitters, and Hormones: Neuroendocrine and Genetic Mechanisms
dc.rightsAcesso restrito
dc.subjectbeta-adrenoceptorsen
dc.subjectstressen
dc.subjectcardiac functionen
dc.subjectadaptive responsesen
dc.titleAdrenoceptors and Adaptive Mechanisms in the Heart during Stressen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.description.affiliationUniversidade Federal de São Paulo, Dept Hlth Sci, BR-11060001 Santos, SP, Brazil
dc.description.affiliationUniv Estadual Campinas, Dept Physiol & Biophys, Inst Biol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Hlth Sci, BR-11060001 Santos, SP, Brazil
dc.identifier.doi10.1196/annals.1410.075
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000262398300044
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