REDUCED SENSITIVITY OF THE RENAL CIRCULATION TO ANGIOTENSIN-II IN PREGNANT RATS

The renal circulation undergoes significant changes during pregnancy a nd pregnancy-induced hypertension. Although numerous studies indicate that the presser response to angiotensin II (Aug II) is reduced during pregnancy, it is unclear as to whether this altered sensitivity to An g II occurs in the renal circulation. The first aim of this study was to determine whether the renal vascular responsiveness to exogenous An g II is altered in the midterm pregnant rat. AU rats were pretreated w ith an intravenous infusion of the converting-enzyme inhibitor captopr il (20 mu g.kg(-1).min(-1)) to block endogenous Ang II formation. Foll owing a control period, Ang II was infused at a dose of 10 ng.kg(-1).m in(-1) for 50 minutes into the renal arteries via a suprarenal aortic catheter. In anesthetized virgin rats, Ang II markedly decreased renal plasma flow (RPF) by 39% (5.0 +/- 0.4 to 3.1 +/- 0.4 mL/min), glomeru lar filtration rate (GFR) by 39% (1.9 +/- 0.1 to 1.16 +/- 0.2 mL/min), and urine flow by 47% (22.1 +/- 5.6 to 12.3 +/- 4.8 mu L/min). In con trast, Ang II had no significant effect on RPF, GFR, and urine flow in the anesthetized pregnant rats. Since nitric oxide (NO) has been prev iously reported to modulate the renal vascular actions of Ang II in no rmal animals and NO synthesis is thought to be elevated in preg nancy, this study examined the role of NO in the attenuated renal response t o Ang II. In pregnant rats pretreated with L-NAME, the arterial pressu re was higher and RPF was lower than in the control pregnant rats. How ever, the renal response to Ang II in the L-NAME-pretreated pregnant r ats was similar to control pregnant rats. These data indicate that the renal circulation has a reduced sensitivity to Ang II during pregnanc y. We also found that NO synthesis inhibition does not alter the atten uated renal response to Ang II in the anesthetized pregnant rats.