SYMPATHETICALLY MEDIATED EFFECTS OF ANGIOTENSIN ON THE DOG HEART IN SITU

¹ Department of Medicine, Cardiac Research Laboratory and Department of Pharmacology, University of Cincinnati, College of Medicine, Cincinnati, Ohio

Angiotensin II increases blood pressure, heart rate and contractile force in the anesthetized dog. The mechanism by which it produces these effects was studied in the dog heart in situ. The positive inotropic and chronotropic responses were not abolished after acute bilateral adrenalectomy or ganglionic blockade, but were markedly reduced by beta adrenergic blockade, reserpine or acute decentralization of the heart either surgically in situ or in the form of a heart-lung preparation. The results suggest that the predominant cardiac effects of angiotensin are not caused by the release of catecholamines into the circulation from the adrenal medulla, stimulation of the central nervous system, direct stimulation of the heart's beta receptors or the local release of catecholamines from the nerve terminals. The evidence suggests that angiotensin, at low doses (1 µg/kg), causes its predominant cardiac effects by the stimulation of the ganglion cells of the cardiac sympathetic nerves even in the presence of ganglionic blockade.