Pressor action and dipsogenicity induced by angiotensin II and III in rats

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Abstract
The primary brain sites responsible for angiotensin-induced pressor action and dipsogenicity in the laboratory rat appear to be located in forebrain circumventricular organs(CVO). Because CVOs have a reduced blood-brain barrier, intracarotid infusion of angiotensin via a brachial arterial catheter results in direct stimulation of these sites. This investigation determined that brachial arterial infusion of angiotensin II (ANG II) into alert free-moving rats resulted in pressor and dipsogenic responses greater than those observed with equivalent doses of angiotensin III (ANG III). However, intracerebroventricular (ICV) injections of ANG II and ANG III yielded equivalent pressor and drinking responses. ICV pretreatment with the specific angiotensin receptor antagonist [Sar1,Ile8]-ANG II significantly reduced ANG II- and ANG III-induced pressor and drinking responses. This inhibition lasted .apprx. 20 min with recovery at 60-70 min. The results indicate that ICV-administered ANG III is a much more potent ligand than previously determined if the stickiness due to electrical charge of this compound is prevented by appropriate treatment of glassware. The receptor antagonist results encourage the possibility that ANG II and ANG III activate a common central receptor site.