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

这项研究的主要结果可归纳如下。首先，我们研究了ANP抑制反射交感神经激活的机制。大鼠的结果表明，静脉内ANP激活迷走神经传入，从而抑制肾和腰交感神经活动（SNA）和ANP重置SNA的动脉压力感受性反射控制到较低的压力范围。第二，我们尝试探讨心钠素对家兔动脉压力感受性反射重置的机制。Anp扩张主动脉，使主动脉降压神经活动不减少，尽管低血压。ANP不改变主动脉直径与主动脉降压神经活动的关系，提示ANP不改变主动脉压力感受器对应变的敏感性。我们还研究了ANP可能通过其对中枢神经系统的影响而改变SNA的可能性。然而，我们没有发现这种可能性的证据。在一项临床研究中，我们检查了心钠素对心力衰竭患者的直接血管舒张作用的大小。与正常人相比，心力衰竭患者心钠素的扩血管作用明显减弱。由于两组间血浆环鸟苷酸随心钠素输注而升高的趋势相似，故心力衰竭时心钠素反应减弱不是由于心钠素受体数量减少，而是由于细胞内异常所致。

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.