Endothelial AT(1) and AT(2) pathways in aortic responses to angiotensin II after stress and ethanol consumption in rats
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Data
2014-12-01
Autores
Ferreira Baptista, Rafaela de Fatima [UNESP]
Chies, Agnaldo Bruno [UNESP]
Taipeiro, Elane de Fatima
Cordellini, Sandra [UNESP]
Título da Revista
ISSN da Revista
Título de Volume
Editor
Informa Healthcare
Resumo
Stress and ethanol are important cardiovascular risk factors. Their vascular and blood pressure (BP) effects were evaluated alone and in combination. Adult male Wistar rats (8-10 per group) were separated into control, ethanol (ethanol 20% in drinking water for 6 weeks), stress (restraint 1 h/d 5 d/week for 6 weeks), and ethanol/stress (in combination) groups. Systolic BP was evaluated weekly. Concentration-response curves for contractile responses to angiotensin II in the absence and the presence of losartan (AT(1)-blocker), PD123-319 (AT(2)-blocker), L-NAME (nitric oxide synthase inhibitor), or indomethacin (cyclooxygenase inhibitor) were obtained in isolated intact and endothelium-denuded aortas. Effective concentration 50% (EC50) and maximum response (MR) were compared among groups using MANOVA/Tukey tests. Stress and stress plus ethanol increased BP. Ethanol and stress, alone and in combination, did not alter angiotensin responses of intact aortas. PD123-319 decreased MR to angiotensin II in intact aortas from the ethanol and ethanol/stress groups relative to control in the presence of PD123-319. Losartan increased MR to angiotensin II in intact aortas from the stress and ethanol/stress groups relative to control in the presence of losartan. None of the protocols altered angiotensin responses of denuded aortas. Neither indomethacin nor L-NAME altered angiotensin responses of intact aortas from the experimental groups. Thus ethanol and ethanol plus stress may alter endothelial signaling via AT(1)-receptors, without changing systemic BP. Stress and stress plus ethanol may alter endothelial signaling via AT(2)-receptors, and thereby increase BP. Knowledge of such vascular changes induced by stress and/or ethanol may contribute to understanding adverse cardiovascular effects of stress and ethanol consumption in humans.
Descrição
Palavras-chave
Angiotensin II, AT(1) and AT(2) pathways, ethanol consumption, nitric oxide, restraint stress, vascular reactivity
Como citar
Stress-the International Journal On The Biology Of Stress. London: Informa Healthcare, v. 17, n. 6, p. 512-519, 2014.