Davison J M, Lindheimer M D
Baillieres Clin Endocrinol Metab. 1989 Aug;3(2):451-72. doi: 10.1016/s0950-351x(89)80011-4.
This chapter reviews alterations in volume and sodium homeostasis and osmoregulation during human pregnancy. Pregnant women undergo extracellular and plasma volume increases of 50-70%, and these changes accompany marked cumulative sodium retention shared by both mother and fetus. Pregnancy alters several factors with opposing effects on renal salt handling; however, mechanisms by which gestational sodium accumulation and volume expansion are achieved remain obscure. Furthermore, despite substantial increases in absolute blood volume, considerable uncertainty exists as to how this volume is sensed, particularly in late pregnancy when a rapid increase in volume is associated with decreases in peripheral resistance and blood pressure. Attempts to assess 'effective' intravascular volume suggest that pregnant women sense their volume as normal. Osmoregulation is also changed. Body tonicity and the osmotic thresholds for AVP release and thirst decrease by about 10 mosm/kg. The mechanisms responsible for the osmoregulatory changes are obscure. Haemodynamic stimuli such as decrements in blood pressure and of 'effective circulating volume' do not seem to account for them. Of the many increments in hormone levels known to accompany gestation, only hCG has so far been implicated in these changes. Pregnant women experience three- to fourfold increments in AVP disposal rates between early and mid pregnancy; this may be caused by the striking rise in circulating cystine-aminopeptidase (vasopressinase) which also occurs during this period. The increments in MCR may be one reason why the hormonal response to a given osmotic stimulus appears to decrease in late pregnancy. All these alterations permit speculation on the manner in which the decrease in Posm occurs and is maintained within narrow limits. Lowering the osmotic threshold to drink stimulates a rise in water intake and dilution of body fluids. Since AVP release is not suppressed at the usual level of hypotonicity, AVP continues to circulate at levels sufficient to permit water retention. Posm continues to decline until it decreases below the new osmotic thirst threshold, when a new steady state is established. At this point water turnover, too, resembles that in the non-pregnant state. The change in MCR and the marked increment in plasma vasopressinase may explain certain observations regarding disordered water metabolism during late pregnancy. These are the transient DI syndromes due either to subclinical hypothalamic disease or to a disorder peculiar to pregnancy which is AVP-resistant but dDAVP-responsive; the latter analogue resists degradation by vasopressinase.
本章回顾了人类孕期容量、钠稳态及渗透调节的变化。孕妇细胞外液和血浆量增加50% - 70%，这些变化伴随着母体和胎儿共同出现的显著累积性钠潴留。孕期改变了几个对肾脏盐处理有相反作用的因素；然而，实现妊娠期钠蓄积和容量扩张的机制仍不清楚。此外，尽管绝对血容量大幅增加，但对于如何感知这一容量仍存在相当大的不确定性，尤其是在妊娠晚期，此时血容量快速增加与外周阻力和血压下降相关。评估“有效”血管内容量的尝试表明，孕妇感觉自己的容量正常。渗透调节也发生了变化。身体张力以及抗利尿激素（AVP）释放和口渴的渗透阈值降低约10 mosm/kg。导致渗透调节变化的机制尚不清楚。诸如血压下降和“有效循环容量”减少等血流动力学刺激似乎无法解释这些变化。在已知伴随妊娠的众多激素水平升高情况中，到目前为止只有人绒毛膜促性腺激素（hCG）与这些变化有关。孕妇在妊娠早期和中期之间AVP清除率增加三到四倍；这可能是由于同期循环中的胱氨酸氨基肽酶（血管加压素酶）显著升高所致。代谢清除率（MCR）的增加可能是妊娠晚期对给定渗透刺激的激素反应似乎降低的原因之一。所有这些变化使得人们可以推测血浆渗透压（Posm）降低的方式以及如何将其维持在狭窄范围内。降低饮水的渗透阈值会刺激水摄入量增加和体液稀释。由于在通常的低渗水平下AVP释放未被抑制，AVP继续以足以允许水潴留的水平循环。Posm持续下降，直到降至新的渗透口渴阈值以下，此时建立新的稳态。此时的水周转率也类似于非孕期。MCR的变化和血浆血管加压素酶的显著增加可能解释了妊娠晚期水代谢紊乱的某些观察结果。这些是由于亚临床下丘脑疾病或妊娠特有的一种疾病导致的短暂性尿崩症综合征，后者对AVP有抵抗但对去氨加压素（dDAVP）有反应；后者类似物抵抗血管加压素酶的降解。
