Amastatin potentiation of drinking induced by blood-borne angiotensin: evidence for mediation by endogenous brain angiotensin.

Angiotensinergic synapses in the central nervous system (CNS) have been proposed to be involved in drinking induced by both intracerebroventricular (i.c.v.) and peripheral administration of angiotensins. In the present studies, we tested this hypothesis with i.c.v. application of amastatin, an aminopeptidase A inhibitor, to block peptide degradation. Potentiation of i.c.v. angiotensin II (Ang II)-induced drinking responses was observed when amastatin and Ang II were administered. Amastatin did not potentiate drinking to carbachol which demonstrates that the enhancement is specific to peptides. Centrally administered amastatin also potentiated drinking following systemic administration of Asn1 angiotensin II. (Asn1 Ang II). The results are consistent with the hypothesis that CNS angiotensin synapses are involved in the dipsogenic response that results from elevated levels of circulating angiotensin.