Atlas S A, Maack T
Cardiovascular Center, Cornell University Medical College, New York, New York.
Endocrinol Metab Clin North Am. 1987 Mar;16(1):107-43.
ANF is a peptide hormone with peripheral and central effects on several physiologic control systems, which suggests broad involvement in the regulation of intravascular volume and cardiovascular homeostasis. ANF acts directly on the kidney to modulate renal vascular resistance, increase glomerular filtration rate, and decrease inner medullary hypertonicity. These hemodynamic effects act in concert to promote marked natriuresis and diuresis and to inhibit renin secretion by the kidney; the potential role of direct effects on tubular transport and on the juxtaglomerular cells remains to be clarified. ANF also inhibits steroidogenesis, most prominently affecting agonist-induced aldosterone biosynthesis by the adrenal cortex. ANF exerts a smooth muscle relaxant effect on isolated vessels constricted with various hormonal agonists. ANF causes especially pronounced antagonism of the adrenal and vascular actions of angiotensin II and antagonizes the latter peptide's central nervous system effects. Although complex systemic hemodynamic mechanisms are involved, ANF-induced vasorelaxation may contribute to its depressor action, particularly in states characterized by angiotensin II-induced vasoconstriction. Distention of the atria is a major stimulus to ANF release and evokes many responses that are mimicked by ANF infusion. Although ANF is not the sole or even dominant mediator of the responses to atrial distention, available data suggest that it plays a role in the renal and hormonal responses to intravascular volume expansion. Definitive assessment of its physiologic and pathophysiologic significance must await development of specific antagonists, but further studies on the mechanisms of action of ANF at the molecular, cellular, and systemic levels are likely to contribute significantly to our understanding of the complex process of volume regulation and cardiovascular homeostasis.
心钠素是一种对多种生理控制系统具有外周和中枢作用的肽类激素，这表明它广泛参与血管内容量调节和心血管稳态维持。心钠素直接作用于肾脏，调节肾血管阻力，增加肾小球滤过率，并降低髓质内高渗性。这些血流动力学效应共同作用，促进显著的利钠和利尿，并抑制肾脏分泌肾素；其对肾小管转运和肾小球旁细胞的直接作用的潜在作用仍有待阐明。心钠素还抑制类固醇生成，最显著地影响肾上腺皮质激动剂诱导的醛固酮生物合成。心钠素对用各种激素激动剂收缩的离体血管具有平滑肌舒张作用。心钠素尤其能显著拮抗血管紧张素II的肾上腺和血管作用，并拮抗后者肽的中枢神经系统作用。尽管涉及复杂的全身血流动力学机制，但心钠素诱导的血管舒张可能有助于其降压作用，特别是在以血管紧张素II诱导的血管收缩为特征的状态下。心房扩张是心钠素释放的主要刺激因素，并引发许多与心钠素输注所模拟的反应。尽管心钠素不是对心房扩张反应的唯一甚至主要介质，但现有数据表明它在对血管内容量扩张的肾脏和激素反应中起作用。对其生理和病理生理意义的明确评估必须等待特异性拮抗剂的开发，但对心钠素在分子、细胞和系统水平作用机制的进一步研究可能会极大地有助于我们理解容量调节和心血管稳态的复杂过程。
