Central angiotensin III-induced dipsogenicity in rats and gerbils

Previous findings from our laboratory demonstrated [125I]angiotensin II (AII) binding to plasma membranes from rat but not gerbil circumventricular organs (CVOs), the presumed location of brain receptors for angiotensin-induced dipsogenicity. Since members of both species drink to intracranially applied AII, a degradation product of AII was suspected to be the active ligand in gerbils. High specific [125I]angiotensin III (AIII) binding capacity was presently determined in CVOs taken from both rats and gerbils. Nearly identical dose-response curves were obtained for members of each species following the intracerebroventricular injection of AIII; however, rats drank more water than gerbils following the administration of AII. These results were interpreted to suggest that the dipsogenically active ligand in gerbils is AIII or derived from AIII, and that this analogue also contributes to angiotensin-induced drinking in rats. Since the distribution of specific angiotensin binding capacity represented by gerbil closely approximates that seen in non-human primate brain, these findings are of particular relevance and encourage future efforts directed toward understanding the role of AII metabolites in the central control of dipsogenicity.