Angiotensin-induced thirst: effects of third ventricle obstruction and periventricular ablation.

The role of periventricular tissue surrounding the anteroventral third ventricle (AV3V) in mediating drinking behavior induced by angiotensin II was investigated rats. Electrolytic lesions which bilaterally destroyed preoptic-hypothalamic periventricular tissue surrounding AV3V abolished drinking responses normally elicited by intracerebral injections of angiotensin. In another experiment, ventricular obstruction in AV3V had no effect on drinking of a palatable sweet milk solution while the drinking responses induced by peripheral versus central administration of angiotensin were dissociated. Drinking normally induced by lateral preoptic injections of angiotensin was no longer observed when AV3V obstruction prevented drug distribution via cerebrospinal fluid circulation to AV3V periventricular tissue; the drinking response induced by subcutaneous injection of angiotensin was enhanced, however, after placement of the ventricular obstruction. These results, coupled with the earlier observation that AV3V lesions also abolish drinking induced by subcutaneous angiotensin injectin, suggest that, after central or peripheral administration, angiotensin acts on AV3V periventricular tissue to arouse drinking. In contrast to centrally injected angiotensin, peripherally administered angiotensin does not contact receptors by entry and spread in cerebrospinal fluid. After peripheral injection angiotensin may contact sensitive AV3V tissue directly from blood, perhaps via the organum vasculosum of the lamina terminalis, a highly vascularized circumventricular organ within the AV3V which lacks a blood-brain barrier.