Gellai M, Allen D E, Beeuwkes R
Fed Proc. 1986 Aug;45(9):2387-91.
In a rather short time, a consensus seems to have emerged among researchers regarding the mechanisms of the natriuretic and hypotensive actions of atrial natriuretic factor (ANF). According to the by now classic view, the natriuresis induced by ANF is mediated by changes in renal hemodynamics; vasorelaxation is proposed as the primary mechanism of its hypotensive action. Recent evidence, mostly from experiments with conscious animals, does not support this view. Results from experiments performed with chronically instrumented spontaneously hypertensive rats and normotensive (Wistar-Kyoto and Wistar) rats show that the natriuresis induced by a synthetic ANF is not accompanied by increases in glomerular filtration rate or renal blood flow. Measurement of cardiac output (CO) and blood pressure indicate that a decrease in CO, not a fall in total peripheral resistance, is the cause of the decrease in blood pressure. Based on this and other available evidence, a hypothetical scheme for the biological role of ANF is proposed.
在相当短的时间内，研究人员似乎已就心钠素（ANF）的利钠和降压作用机制达成了共识。根据目前的经典观点，ANF诱导的利钠作用是由肾血流动力学变化介导的；血管舒张被认为是其降压作用的主要机制。然而，最近的证据，大多来自清醒动物实验，并不支持这一观点。对慢性植入仪器的自发性高血压大鼠和正常血压（Wistar-Kyoto和Wistar）大鼠进行的实验结果表明，合成ANF诱导的利钠作用并未伴随着肾小球滤过率或肾血流量的增加。心输出量（CO）和血压的测量表明，血压下降的原因是CO降低，而非总外周阻力下降。基于这一证据及其他现有证据，提出了一个关于ANF生物学作用的假说方案。
