Reduced uterine perfusion pressure during pregnancy in the rat is associated with increases in arterial pressure and changes in renal nitric oxide

A reduction in nitric oxide (NO) synthesis has been suggested to play a rol e 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 sy nthase. The purpose of this study was to determine whether whole-body and r enal NO production is reduced in a rat model of pregnancy-induced hypertens ion produced by chronically reducing uterine perfusion pressure starting at day 14 of gestation. Chronic reductions in uterine perfusion pressure resu lted in increases in arterial pressure of 20 to 25 mm Hg, decreases in rena l plasma flow (< 23%) and glomerular filtration rare (< 40%), but no differ ence in urinary nitrite/nitrate excretion relative to control pregnant rats . In contrast, reductions in uterine perfusion pressure in virgin rats resu lted in no significant effects on arterial pressure. Renal endothelial (<4% ) and inducible (< 11%) NO synthase protein expression did not decrease sig nificantly in the chronically reduced uterine perfusion pressure rats relat ive to normal pregnant rats; however, significant reductions in neuronal NO synthase were observed (< 30%). The results of this study indicate that th e reduction in renal hemodynamics and the increase in arterial pressure obs erved in response to chronic decreases in uterine perfusion pressure in pre gnant rats are associated with no change in whole-body NO production and a decrease in renal protein expression of neuronal NO synthase.