Schrier R W, Howard R L
Department of Medicine, University of Colorado School of Medicine, Denver 80262.
Nihon Naibunpi Gakkai Zasshi. 1989 Dec 20;65(12):1311-27. doi: 10.1507/endocrine1927.65.12_1311.
Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
钠和水潴留是包括心力衰竭、肝硬化、肾病综合征及妊娠等水肿性疾病的特征。近年来，利用一种灵敏的血浆血管加压素放射免疫测定法发现，非渗透性血管加压素释放参与了这些水肿性疾病的水潴留过程。在实验研究及人体研究中发现，血管加压素的非渗透性释放始终与交感神经系统及肾素 - 血管紧张素 - 醛固酮系统的激活相关。此外，已表明交感神经系统参与血管加压素的非渗透性释放（颈动脉和主动脉压力感受器）及肾素 - 血管紧张素系统的激活（肾β - 肾上腺素能受体）。这些发现促使我们提出，体液容量调节涉及心输出量与外周动脉阻力之间的动态相互作用。在此背景下，细胞外液总量（ECF）及血容量均非肾钠和水排泄的决定因素。相反，肾钠和水潴留要么由心输出量下降（如ECF容量减少、低输出量心力衰竭、心包填塞或低血容量性肾病综合征）引发，要么由外周动脉血管舒张引发（如高输出量心力衰竭、肝硬化、妊娠、脓毒症、动静脉瘘及药物性血管扩张剂）。随着有效动脉血容量（EABV）因心输出量下降或外周动脉血管舒张而减少，急性反应涉及由血管紧张素、交感神经介质及血管加压素介导的血管收缩。恢复EABV的较慢反应涉及血管加压素介导的水潴留及醛固酮介导的钠潴留。伴随那些通过降低心输出量或引起外周动脉血管舒张而使EABV减少的状态出现的肾血管收缩，限制了远端肾小管钠和水的输送，从而使血管加压素的保水作用最大化，并削弱了对醛固酮钠潴留作用的正常逃逸。妊娠时肾小球滤过率及滤过钠负荷升高，尽管EABV减少，但仍可增加远端钠和水的输送，从而限制妊娠期水肿的形成。
