Pulse exposure to ethanol augments vascular contractility through stress response
The Korean Journal of Physiology and Pharmacology
; : 47-53, 2001.
Article
em En
| WPRIM
| ID: wpr-728115
Biblioteca responsável:
WPRO
ABSTRACT
Drinking excessive alcohol has been recognized as a risk factor for hypertension. However, the mechanism by which alcohol intake causes hypertension still remains elusive. We tested the hypothesis that ethanol itself acts as a stress factor on vasculature and indirectly modulates vascular contractility. After end of exposure to 1, 2.5 and 5% ethanol for 45 min, rat aortic strips were subjected to contractile responses, immunoblot for Hsp70 and the measurement of levels of myosin light chain phosphorylation. Exposure to 5% ethanol not only augmented contractions to KCl or phenylephrine, but also increased expression of Hsp70 and the levels of myosin light chain phosphorylation. There were no significant differences in contractions produced by 1 micromol/L phorbol 12,13-dibutyrate, a protein kinase C activator, whether the tissues were exposed to 5% ethanol or not. This is the first report to show that even short exposure to ethanol has a delayed effect to increase vascular smooth muscle contractility through a modulation of thick filament regulation. It may be a mechanism by which ingestion of alcohol induces hypertension.
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Fenilefrina
/
Fosforilação
/
Proteína Quinase C
/
Dibutirato de 12,13-Forbol
/
Fatores de Risco
/
Cadeias Leves de Miosina
/
Etanol
/
Ingestão de Líquidos
/
Ingestão de Alimentos
/
Hipertensão
Tipo de estudo:
Etiology_studies
/
Risk_factors_studies
Limite:
Animals
Idioma:
En
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
2001
Tipo de documento:
Article