Schrier R W, Dürr J A
Am J Kidney Dis. 1987 Apr;9(4):284-9. doi: 10.1016/s0272-6386(87)80123-3.
With pregnancy, the expansion of plasma and extracellular fluid volume, increased cardiac output, and increased glomerular filtration rate (GFR) and renal blood flow (RBF) are compatible with primary renal sodium and water retention with secondary enlargement of the vascular compartment (overfill hypothesis). Alternatively, a primary enlargement of the vascular compartment (eg, prostaglandin-mediated vasodilation and placental arteriovenous shunting) with secondary renal sodium and water retention (underfill hypothesis) is supported by the activation of the renin-angiotensin-aldosterone (RAA) system, resetting of vasopressin release and thirst to a lower plasma osmolality, and a further stimulation of the RAA system and vasopressin when pregnant rats' water intake is maintained at a level of a virgin rat fluid intake, diminished BP and increased cardiac output in the first trimester, and worsening of hyponatremia with sodium restriction in the pregnant but not the virgin rat. With the underfill hypothesis, normal sodium and water excretion with mineralocorticoid escape could be mediated by hormonally induced increases in GFR and RBF associated with pregnancy. The nature of such a hormone effect of pregnancy to enhance renal hemodynamics remains to be defined.
在妊娠期间，血浆和细胞外液量的增加、心输出量的增加以及肾小球滤过率（GFR）和肾血流量（RBF）的增加与原发性肾钠和水潴留以及血管腔室的继发性扩大（充盈过度假说）是相符的。另外，血管腔室的原发性扩大（例如，前列腺素介导的血管舒张和胎盘动静脉分流）伴继发性肾钠和水潴留（充盈不足假说）得到肾素-血管紧张素-醛固酮（RAA）系统激活、血管加压素释放和口渴阈值重置为较低血浆渗透压的支持，并且当妊娠大鼠的水摄入量维持在未孕大鼠液体摄入量水平时，RAA系统和血管加压素会进一步受到刺激，妊娠早期血压降低和心输出量增加，以及妊娠大鼠而非未孕大鼠在限钠时低钠血症恶化。根据充盈不足假说，盐皮质激素逃逸导致的正常钠和水排泄可能由妊娠相关的激素诱导的GFR和RBF增加介导。妊娠增强肾血流动力学的这种激素效应的性质仍有待确定。
