The renin-angiotensin system and thirst: some unanswered questions

Recent experiments dispute the significance of four findings that usually are cited to support the hypothesis that angiotensin is a natural dipsogen. First, although administration of exogenous renin consistently increases water intake, the plasma renin activities that are produced seem to be outside of the normal physiological range when the elicited drinking is substantial. Second, although plasma renin activities are elevated following caval ligation, colloid, or isoproterenol treatment, this activity of the renin-angiotensin system appears to account for only a small portion of the observed water intake. Third, although bilateral nephrectomy abolishes the water intake that otherwise occurs after caval ligation or isoproterenol treatment, the observed blood pressure appears to be so low as to preclude drinking behavior. Finally, although drinking can be stimulated in these hypotensive rats by various treatments, in each case a pressor response also is observed that might have restored the ability to drink. These new observations have provoked a reevaluation of the circumstances in which endogenous angiotensin stimulates thirst and the magnitude of its contribution then. At present, there is no persuasive evidence that the renin-angiotensin system normally plays a direct and substantial role in mediating the ingestion of water or saline.