Blood-borne and cerebral angiotensin and the genesis of salt intake.

These experiments reevaluate earlier work in which salt intake was evoked by blood-borne angiotensin II. That work is inconsistent with recent demonstrations that cerebral, not blood-borne, angiotensin II is the synergist with aldosterone in arousing salt intake in the rat. We show, first, that the pharmacological doses of angiotensin II that were used in the earlier work are natriuretic (and dipsogenic). They cause urinary sodium losses that precede and exceed sodium intake. Second, we show that the excess sodium intake that is associated with pharmacological doses of intravenous angiotensin is not caused by endogenous aldosterone. Last, we show that this excess sodium intake is abolished by intracerebroventricular captopril thereby suggesting that it is caused by activation of cerebral angiotensin II and harmonizing its mechanism with current concepts.