Baylis C, Reckelhoff J F
Department of Physiology, West Virginia University, Morgantown.
Am J Kidney Dis. 1991 Feb;17(2):98-104. doi: 10.1016/s0272-6386(12)81111-5.
Rats are an excellent animal model in which to study the changes in renal hemodynamics associated with normal pregnancy. Midterm pregnant rats exhibit a maximal renal vasodilation leading to increases in glomerular filtration rate (GFR) and renal plasma flow (RPF). Micropuncture studies in midterm pregnant Munich-Wistar rats have shown that single-nephron GFR (SNGFR) increases, due entirely to increases in plasma flow and, importantly, glomerular capillary blood pressure (PGC) remains unchanged in normotensive pregnancy, due to parallel and proportionally similar reductions in preglomerular (RA) and efferent (RE) arteriolar resistance. Despite the chronic gestational renal vasodilation, pregnancy in normotensive rats with either normal kidneys or a variety of underlying diseases, causes no adverse changes in renal function, perhaps because the glomeruli are protected from damaging high PGC. In the presence of systemic hypertension, the renal vasodilation of pregnancy could put the maternal kidney at risk of injury due to increases in PGC. There are few renal functional studies in preexisting, essential hypertension, but micropuncture studies in spontaneously hypertensive rats (SHRs) have shown that repetitive pregnancies in SHRs cause no functional impairment. Surprisingly, SHRs demonstrated no gestational renal vasodilation, although gestational decreases in peripheral resistance certainly occur in the SHR. This absence of gestational renal vasodilation may be a protective mechanism; it remains to be determined whether hypertensive states in which renal vasodilation does occur are associated with increased risk to the maternal kidney.
大鼠是研究正常妊娠相关肾血流动力学变化的优秀动物模型。妊娠中期的大鼠表现出最大程度的肾血管舒张,导致肾小球滤过率(GFR)和肾血浆流量(RPF)增加。对妊娠中期的慕尼黑-维斯塔尔大鼠进行的微穿刺研究表明,单肾单位GFR(SNGFR)增加,这完全是由于血浆流量增加所致,重要的是,在血压正常的妊娠中,肾小球毛细血管血压(PGC)保持不变,这是由于入球小动脉(RA)和出球小动脉(RE)阻力平行且成比例地相似降低。尽管存在慢性妊娠期肾血管舒张,但血压正常且肾脏正常或患有各种基础疾病的大鼠妊娠时,肾功能不会出现不良变化,这可能是因为肾小球受到保护,免受高PGC的损害。在存在系统性高血压的情况下,妊娠时的肾血管舒张可能会因PGC升高而使母体肾脏有受伤的风险。在已存在的原发性高血压中,很少有肾功能研究,但对自发性高血压大鼠(SHR)的微穿刺研究表明,SHR多次妊娠不会导致功能损害。令人惊讶的是,SHR没有出现妊娠期肾血管舒张,尽管SHR的外周阻力在妊娠期肯定会降低。这种妊娠期肾血管舒张的缺失可能是一种保护机制;肾血管舒张确实发生的高血压状态是否与母体肾脏风险增加相关,仍有待确定。