ANP plays an important role in cardiovascular regulation by inhibiting sympathetic nerve activity and augmenting parasympathetic effects on heart rate, in addition to its direct vasodilating and renal effects.
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Supports integrated view of ANP in autonomic regulation; leaves open whether these effects translate to improved outcomes in cardiovascular disease.
Hypotension caused by atrial natriuretic peptide (ANP) is often not accompanied by the anticipated increases in heart rate or sympathetic nerve activity. The sympathetic inhibitory action of ANP occurs in cardiac and noncardiac sympathetic nerves, and has been demonstrated in conscious or anesthetized animals as well as in humans. The sympathetic inhibition by ANP occurs after atropinization but is abolished after vagotomy. Thus, ANP alters sympathetic nerve activity by influencing cardiopulmonary baroreceptors, which in turn is mediated by vagal afferents. In addition to the effects of ANP on cardiopulmonary baroreceptors, ANP affects arterial baroreceptors. ANP dilates the ascending aorta where some of the arterial baroreceptors are located, causing resetting of these arterial baroreceptors. When ANP is microinjected into the cerebroventricle or nucleus tractus solitarii, it causes inhibition of sympathetic nerve activity. It has been shown that ANP inhibits sympathetic ganglionic transmission and augments cardiac parasympathetic effects on heart rate. Thus, ANP may play important roles in cardiovascular regulation by influencing sympathetic nerve activity and heart rate in addition to the direct vasodilating and renal effects.
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Imaizumi et al. (1993) studied this question.
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