Cardiac Action of Vasoactive Polypeptides in the Rat

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Abstract
Intravenous injection of bradykinin in ganglionically blocked rats has a predominantly pressor effect, instead of the depressor effect it is known to have in unblocked rats. Intra-arterial injection of bradykinin (0.01 to 0.02 µg) either before or after blockade produced a decrease of pressure in the hind limb perfused at a constant rate with autogenous blood. The response of the vascular bed was directly proportional to the perfusion pressure, but at a given pressure no difference was seen between blocked and unblocked animals. At the IV infusion rates used (12.5 and 25 µg/kg/min), bradykinin produced a large increase of CO. Because this action remains after autonomic blockade, it seems probable that its mechanism of action is largely independent of the carotid baroreceptor system. Bradykinin caused a slight increase in heart rate and a marked increase in stroke volume, apparently by a direct effect on the heart. In the blocked animal the vasodilator effect of bradykinin is less than its cardiac stimulating action and the resulting effect is an elevation of arterial pressure. Angiotensin in the rat has twofold action: a constrictor effect on the arterioles, and a stimulating effect on the heart. The vasoconstrictor effect is direct, unmodified by denervation or by sympathetic blockade. In the intact rat the cardiac action is masked by the activation of the baroreceptor mechanism which overrides the direct cardiac action and causes a decrease in CO. After autonomic blockade the cardiac action of angiotensin becomes apparent and an increase of CO is seen, while changes in TPR remain similar to those of unblocked animals. Since the CO effect cannot be explained by changes in HR and CVP, it appears that angiotensin has a positive isotropic action. In blocked, reserpinized animals angiotensin infusion causes no significant change in CO. These results suggest that catecholamines account for at least part of the cardiac activity of angiotensin.