Beta-adrenergic thirst and its relation to the renin-angiotensin system

Isoproterenol is a potent dipsogen and antidiuretic agent. It also stimulates the release of renin from the kidney. Evidence is presented to substantiate the view that the drinking and increased vasopressin release that follow the systemic injection of a small dose of isoproterenol are mediated via increased activity of the renin-angiotensin system. Larger doses of isoproterenol, which have profound effects on the cardiovascular system, cause drinking and vasopressin release by mechanisms that do not depend solely on the renin-angiotensin system. Other experiments discussed do not support the hypothesis that hypothalamic beta-adrenergic neurons are important in facilitating thirst. Low doses of isoproterenol are more effective in causing drinking and vasopressin release when given peripherally rather than centrally. Evidence is discussed that supports the view that isoproterenol given centrally leaks into the periphery and causes release of renin and subsequent stimulation of drinking and vasopressin release.