Pulse exposure to ethanol augments vascular contractility through stress response.
- Author:
Eun Kyoung YANG
1
;
In Kyeom KIM
Author Information
1. Department of Pharmacology, Kyungpook National University School of Medicine, 101 Dongin-2-Ga, Taegu, South Korea. inkim@knu.ac.kr
- Publication Type:Original Article
- MeSH:
Animals;
Drinking;
Eating;
Ethanol*;
Hypertension;
Muscle, Smooth, Vascular;
Myosin Light Chains;
Phenylephrine;
Phorbol 12,13-Dibutyrate;
Phosphorylation;
Protein Kinase C;
Rats;
Risk Factors
- From:The Korean Journal of Physiology and Pharmacology
2001;5(1):47-53
- CountryRepublic of Korea
- Language:English
-
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.
