Alcohol satiety, hypertension and the renin-angiotensin system.
Evidence is presented which supports the hypothesis that the renin-angiotensin (r-a) system regulates alcohol intake. Documented findings suggest that an elevated level of r-a activity represents a satiety signal which stops alcohol intake. The fact that alcohol itself is known to stimulate r-a activity suggests that its intake may in some sense be self-regulating and that levels of r-a activity below those which signal satiety may even be rewarding. The role of the r-a system in hypertension is also considered. The ability of alcohol to elevate r-a activity may be seen as a contributing factor to alcohol-induced hypertension because angiotensin is a potent pressor agent. Furthermore, the notion that lower levels of angiotensin may be rewarding permits the hypothesis that essential hypertension may, in part, be the result of a self-induced increase in endogenous angiotensin. This would explain the otherwise puzzling utility of the angiotensin converting enzyme inhibitors in the treatment of essential hypertension.
Grupp
L A
LA
Department of Pharmacology, University of Toronto, Ontario, Canada.
D000428:Alcohol Drinking / Q000502:physiology*; D000437:Alcoholism / Q000150:complications; D000818:Animals; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D008954:Models, Biological; D051381:Rats; D012084:Renin-Angiotensin System; D012527:Satiation / Q000502:physiology*