Abstract
In this review, the site and mode of action of A[angiotensin]II in the brain was considered and the evidence for and against the brain-iso-renin-angiotensin system was discussed. When injected into the brain AII produces drinking behavior, a blood pressure increase and vasopressin release. These effects differ in certain respects from responses to i.v. AII. A major question still unresolved is whether i.v. AII acts on the same receptor sites as ivt [intraventricular] AII. While studies with Saralasin indicate that they do, newer evidence from a horseradish peroxidase experiment on the BBB indicates that at low doses of the agonist or antagonist the i.v. and ivt routes are separate. AII is most effective when injected into the ventricles, and attention has been focused on 2 circumventricular organs as receptor sites: the SFO [subfornical organ] and the OV [organum vasculosum]. There are several lines of evidence for both sites having receptors for AII. While the SFO may be a receptor to plasma-borne AII the OV appears available to both plasma-borne AII and CSF-borne AII. The high sensitivity of a receptor to AII from another source than renal renin raises the question of whether it serves as a receptor for endogenous brain angiotensin.