Intracerebroventricular and systemic saralasin used to investigate angiotensin-elicited activation of the pituitary-adrenocortical axis in the goat.

Intracerebroventricular (ICV) infusion of the competitive inhibitor for angiotensin II (AII), saralasin, (13 pmol kg-1 min-1), preceding and outlasting the intravenous (i.v.) infusion of AII (40 pmol kg-1 min-1) extinguished the elevation in plasma cortisol (PC) obtained in response to just the i.v. AII infusion. The corresponding i.v. infusion of saralasin did not visibly influence the AII-induced elevation of PC, whereas bilateral intracarotid infusions of the inhibitor tended to reduce the response. The ICV administration of the inhibitor also significantly reduced the rise in plasma aldosterone (PA) seen as an effect of the i.v. AII. Paradoxically, however, the intravascular infusions of saralasin conspicuously augmented the rise in PA obtained after the simultaneous i.v. infusion of AII. It is concluded that cerebral mediation of the ACTH-cortisol response to systemic AII occurs at sites accessible to inhibition from both sides of the blood-brain barrier, and that also the PA response to blood-borne AII may be to some extent cerebrally mediated.