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.