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Central component of the cario-accelerator action of angiotensin II in dogs.

Injection of angiotensin II into a lateral cerebral ventricle (I.C.V.) or into a peripheral vein of anaesthetized dog elicited a rise in blood pressure and transient bradycardia followed by sustained tachycardia. Spinal transection at C2 and bilateral vagotomy abolished the central cardiovascular effect of I.C.V. angiotensin. However, in spinal transected dogs the usual pressor response to intravenous angiotensin was observed. Since the transient bradycardia was absent in bilaterally vagotomized dogs or in dogs with their blood pressure stabilized by means of a mechanical buffer devise it must be reflex in origin. The tachycardia was more marked in vagotomized dogs. Prior administration of a beta adrenergic receptor blocking agent propranolol, blocked the tachycardia, but the pressor response was unaffected. The cardiovascular responses to centrally administered angiotensin were practically abolished by prior treatment of dogs with reserpine or by extirpation of both adrenal glands. Thus it may be concluded that ICV angiotensin induces a centrogenic release of catecholamines from the adrenal medulla which is responsible for the cardiovascular responses.