Lindheimer M D, Barron W M, Davison J M
Department of Obstetrics and Gynecology, University of Chicago, IL.
Am J Kidney Dis. 1991 Feb;17(2):105-11. doi: 10.1016/s0272-6386(12)81112-7.
This article, a review of factors controlling vasopressin (AVP) release in pregnancy, extends our contribution to a symposium in this journal published in 1987 (vol X, pp 270-275). Body tonicity decreases (approximately 10 mOsm/kg) very early in pregnancy due to decrements in the osmotic thresholds for AVP release and thirst. In addition, the metabolic clearance rate (MCR) of AVP markedly increases between gestational week 10 and midpregnancy, and is paralleled by the appearance and increase of circulating cystine aminopeptidase (vasopressinase), while the MCR of 1-deamino-8-D-AVP (DDAVP), an analogue resistant to inactivation by the enzyme, changes little in pregnancy. These increases (MCR of AVP and plasma vasopressinase) may explain certain syndromes of transient diabetes insipidus (DI) that complicate gestation. Finally, mechanisms responsible for the altered osmoregulation in pregnancy are obscure, but chorionic gonadotropin may be involved in the changes during human gestation.
本文是一篇关于孕期控制血管加压素（AVP）释放的因素的综述，扩展了我们对该杂志1987年发表的一次研讨会的贡献（第十卷，第270 - 275页）。由于AVP释放和口渴的渗透阈值降低，孕期早期机体张力降低（约10 mOsm/kg）。此外，在妊娠第10周与妊娠中期之间，AVP的代谢清除率（MCR）显著增加，同时循环中的胱氨酸氨基肽酶（血管加压素酶）出现并增加，而1 - 去氨基 - 8 - D - AVP（DDAVP），一种对该酶失活有抗性的类似物，其MCR在孕期变化不大。这些增加（AVP的MCR和血浆血管加压素酶）可能解释了一些使妊娠复杂化的短暂性尿崩症（DI）综合征。最后，孕期渗透压调节改变的机制尚不清楚，但绒毛膜促性腺激素可能参与了人类妊娠期间的这些变化。
