Adrenoceptors and Adaptive Mechanisms in the Heart during Stress

Adrenoceptors and Adaptive Mechanisms in the Heart during Stress

Author Spadari-Bratfisch, Regina Celia Autor UNIFESP Google Scholar
Santos, Iraides Nunes dos Google Scholar
Kvetnansky, R. Google Scholar
Aguilera, G. Google Scholar
Goldstein, D. Google Scholar
Jezova, D. Google Scholar
Krizanova, O. Google Scholar
Sabban, E. L. Google Scholar
Pacak, K. Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Universidade Estadual de Campinas (UNICAMP)
Abstract Several 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.
Keywords beta-adrenoceptors
Cardiac function
Adaptive responses
Language English
Date 2008-01-01
Published in Stress, Neurotransmitters, and Hormones: Neuroendocrine and Genetic Mechanisms. Oxford: Blackwell Publishing, v. 1148, p. 377-383, 2008.
ISSN 0077-8923 (Sherpa/Romeo, impact factor)
Publisher Blackwell Publishing
Extent 377-383
Access rights Closed access
Type Article
Web of Science ID WOS:000262398300044

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