The role of atrial natriuretic peptide in control of circulation and body fluid in heart failure

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The major findings of this study may be summarized as follows. First, we examined the mechanisms by which ANP inhibits reflex sympathetic activation. The results in rats indicated that intravenous ANP activated vagal afferents and thereby inhibited renal and lumbar sympathetic nerve activity (SNA) and that ANP reset arterial baroreflex control of SNA to a lower pressure range. Second, we attempted to explore the mechanisms of the reset of arterial baroreceptor reflex by anp in rabbits. Anp dilated the aorta so that aortic depressor nerve activity did not decrease despite hypotension. Anp did not alter the relationship between aortic diameter ANP aortic depressor nerve actvity, which suggested that anp did not change sensitivity of aortic baroreceptor to strain. We also examined the possibility that ANP may alter SNA by its effect on the central nervous system. However, we did not find evidence suggestive of such possibility. In a clinical study, we examined the magnitude of direct vasodilator effect of ANP in patients with heart failure. As compared to those in normal subjects, the vasodilating effect of ANP was markedly attenuated in patients with heart failure. Since the increases in plasma cyclic GMP with infusion of ANP were similar between the two groups, the attenuated response to ANP in heart failure ded not result from decreased numbers of ANP receptors but was due to intracellular abnormality.