Alexander B T, Kassab S E, Miller M T, Abram S R, Reckelhoff J F, Bennett W A, Granger J P
Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
Hypertension. 2001 Apr;37(4):1191-5. doi: 10.1161/01.hyp.37.4.1191.
A reduction in nitric oxide (NO) synthesis has been suggested to play a role in pregnancy-induced hypertension. We have recently reported that normal pregnancy in the rat is associated with significant increases in whole-body NO production and renal protein expression of neuronal and inducible NO synthase. The purpose of this study was to determine whether whole-body and renal NO production is reduced in a rat model of pregnancy-induced hypertension produced by chronically reducing uterine perfusion pressure starting at day 14 of gestation. Chronic reductions in uterine perfusion pressure resulted in increases in arterial pressure of 20 to 25 mm Hg, decreases in renal plasma flow (<23%) and glomerular filtration rate (<40%), but no difference in urinary nitrite/nitrate excretion relative to control pregnant rats. In contrast, reductions in uterine perfusion pressure in virgin rats resulted in no significant effects on arterial pressure. Renal endothelial (<4%) and inducible (<11%) NO synthase protein expression did not decrease significantly in the chronically reduced uterine perfusion pressure rats relative to normal pregnant rats; however, significant reductions in neuronal NO synthase were observed (<30%). The results of this study indicate that the reduction in renal hemodynamics and the increase in arterial pressure observed in response to chronic decreases in uterine perfusion pressure in pregnant rats are associated with no change in whole-body NO production and a decrease in renal protein expression of neuronal NO synthase.
一氧化氮（NO）合成减少被认为在妊娠高血压综合征中起作用。我们最近报道，大鼠正常妊娠与全身NO生成及神经元型和诱导型NO合酶的肾蛋白表达显著增加有关。本研究的目的是确定在妊娠第14天开始通过长期降低子宫灌注压产生的妊娠高血压大鼠模型中，全身和肾脏的NO生成是否减少。长期降低子宫灌注压导致动脉压升高20至25 mmHg，肾血浆流量降低（<23%）和肾小球滤过率降低（<40%），但与对照妊娠大鼠相比，尿亚硝酸盐/硝酸盐排泄无差异。相反，未孕大鼠子宫灌注压降低对动脉压无显著影响。与正常妊娠大鼠相比，长期降低子宫灌注压大鼠的肾内皮型（<4%）和诱导型（<11%）NO合酶蛋白表达未显著降低；然而，观察到神经元型NO合酶显著降低（<30%）。本研究结果表明，妊娠大鼠长期子宫灌注压降低导致的肾血流动力学降低和动脉压升高与全身NO生成无变化及肾神经元型NO合酶蛋白表达降低有关。
