Mechanisms of the central pressor action of angiotensin II in conscious rats.

Previous studies have demonstrated that, due to a central action, angiotensin II (ANG II) infused via the carotid artery of the rat elicited a greater pressor response than ANG II infused via the abdominal aorta. In the present study, regional vascular resistance responses to carotid and abdominal aortic infusions of ANG II and angiotensin I (ANG I) were compared in conscious unrestrained rats. Miniaturized pulsed Doppler flow probes were used to record regional blood flows. Carotid and aortic infusions caused vasoconstriction in the hindquarters, renal, and mesenteric vascular beds; the carotid route resulted in greater increases in arterial pressure and regional vascular resistances. The enhanced vasoconstrictor responses to carotid infusions of ANG II were significantly attenuated by systemic hexamethonium or central saralasin. Unlike ANG II, carotid and aortic infusions of ANG I produced equivalent regional vasoconstrictor responses not affected by central saralasin. It is concluded that in addition to its peripheral effects, central actions of ANG II induce neurally mediated vasoconstriction of the hindquarters, renal, and mesenteric vascular beds. Central effects of ANG II do not appear to result from conversion in the brain of blood-borne ANG I.