Schrier Robert W
Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado, USA.
Am J Med. 2006 Jul;119(7 Suppl 1):S47-53. doi: 10.1016/j.amjmed.2006.05.007.
This article discusses the pathophysiology of sodium and water retention in edematous disorders with a particular focus on cardiac failure, cirrhosis, and pregnancy. The body fluid volume hypothesis, which emphasizes the dominant role of arterial baroreceptors in renal sodium and water excretion, is reviewed. With arterial underfilling, either due to a decrease in cardiac output or peripheral arterial vasodilation, the normal central inhibition of the sympathetic nervous system activity and baroreceptor-mediated, nonosmotic arginine vasopressin (AVP) release is attenuated. The resultant increase in renal adrenergic activity stimulates the renin-angiotensin-aldosterone system. Although the resultant increase in systemic vascular resistance compensates for the primary arterial underfilling, this activation of the neurohumoral axis results in diminished sodium and water delivery to the renal collecting duct sites of aldosterone, AVP, and natriuretic peptide action. This diminished distal sodium and water delivery will be discussed as an important factor in the failure to escape from the sodium-retaining effects of aldosterone, the resistance to the natriuretic and diuretic effects of natriuretic peptides, and the diminished maximal solute-free water excretion in patients with edema. The role of the nonosmotic AVP release in water retention and hypo-osmolality/hyponatremia has been demonstrated in patients and experimental animals by administering nonpeptide, orally active vasopressin V2 receptor antagonists. These agents have been found to increase solute-free water excretion in patients with water-retaining, hyponatremic edema as well as in experimental animals.
本文讨论水肿性疾病中钠水潴留的病理生理学，特别关注心力衰竭、肝硬化和妊娠。本文回顾了强调动脉压力感受器在肾钠水排泄中主导作用的体液容量假说。由于心输出量减少或外周动脉血管舒张导致动脉充盈不足时，交感神经系统活动的正常中枢抑制以及压力感受器介导的非渗透性精氨酸血管加压素（AVP）释放减弱。由此导致的肾肾上腺素能活性增加刺激肾素-血管紧张素-醛固酮系统。虽然由此导致的全身血管阻力增加可补偿原发性动脉充盈不足，但这种神经体液轴的激活会导致输送到醛固酮、AVP和利钠肽作用的肾集合管部位的钠和水减少。这种远端钠和水输送减少将被视为醛固酮钠潴留作用无法消除、对利钠肽利钠和利尿作用产生抵抗以及水肿患者最大无溶质水排泄减少的一个重要因素。通过给予非肽类口服活性血管加压素V2受体拮抗剂，已在患者和实验动物中证实非渗透性AVP释放在水潴留和低渗/低钠血症中的作用。这些药物已被发现可增加水潴留性低钠血症水肿患者以及实验动物的无溶质水排泄。
