The administration of angiotensin II to an animal with intact baroreceptor reflexes results in reflex bradycardia in response to the marked vasoconstriction. When baroreceptor reflexes are depressed (barbiturate anesthesia) or if vagal tone is inhibited (atropine or vago-tomy), angiotensin directly induces cardiac acceleration.
Angiotensin II stimulates the influx of Ca++ into cardiac muscle cells and can exert a direct inotropic effect at cardiac muscle. In addition, angiotensin II can stimulate the sympathoadrenal system and thereby increase myocardial contractility. In contrast to its effects on vascular smooth muscle, the ability of angiotensin to increase the contractile force of the heart is far less potent. Therefore, in spite of the positive chronotropic and inotropic effects produced by angiotensin II, cardiac output is rarely increased. In fact, angiotensin II may decrease cardiac output through reflex bradycardia induced by the rise in peripheral resistance that it causes. In contrast, centrally administered angiotensin II increases both blood pressure and cardiac output.
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