Peripheral adrenergic basis for cardioaccelerator action of angiotensin

Abstract

In dogs which had received morphine sulfate (3 mg/kg), chloralose (90 mg/kg), and tetraethylammonium chloride in doses sufficient to prevent neural influences on heart rate, combined halved doses of synthetic angiotensin (hypertensin, Ciba) and norepinephrine produced the same degree of caridac acceleration as the average of the full equiaccel-erator doses of the two agents. This indicates that there is no significant degree of sensitization by either agent to the cardioaccelerator action of the other. Injection of 1 [mu]g/kg of angiotensin into the left ventricle of dogs which had received tetraethylammonium chloride caused greater cardiac acceleration after a shorter latent period than that which resulted from injections into the right atrium, and injections into the abdominal aorta produced less than half of the maximum acceleration that resulted from injections into the right atrium. Bilateral adrenalectomy did not cause a significan? change in the cardioaccelerator response to angiotensin injected into the left ventricle of dogs under the influence of tetraethylammonium chloride. The acceleration is largely catecholamine dependent, since it is prevented by bretylium tosylate or beta receptor blocking agents. It is concluded that one of the actions of angiotensin is to cause liberation of catecholamines from extra-adrenal sources.