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Title: Cyclooxygenase products do not contribute to the gestational renal vasodilation in the nitric oxide synthase inhibited pregnant rat. Author: Baylis C. Journal: Hypertens Pregnancy; 2002; 21(2):109-14. PubMed ID: 12175438. Abstract: OBJECTIVE: To determine whether vasodilatory cyclooxygenase (COX) products are activated in kidney during chronic nitric oxide synthase inhibition (NOSI) in pregnant rats. METHODS: Chronically catheterized pregnant and nonpregnant Sprague-Dawley female rats were treated with daily NOSI ( L-NAME; 100 mg/L drinking water) for 14 days. Renal function experiments were conducted twice at 7-9 days of chronic NOSI (equivalent to midterm in pregnant rats) and after 14 days (equivalent to late pregnancy). Measurements were made of arterial blood pressure (BP) and renal hemodynamics, specifically glomerular filtration rate (GFR), renal plasma flow (RPF), and renal vascular resistance (RVR), in control and then during acute COX inhibition with indomethacin (2 mg/kg i.v.). RESULTS: Chronic NOSI increased BP and RVR in both virgin and pregnant rats. The normal midterm renal vasodilation was prevented and there was no BP or renal hemodynamic response to acute COX inhibition. By late pregnancy, RPF had fallen further and again, acute COX inhibition had no impact on renal hemodynamics, although a small reduction was seen in GFR in LV. CONCLUSIONS: Vasodilatory COX products cannot compensate for nitric oxide as the renal vasodilatory factor of pregnancy in the rat.[Abstract] [Full Text] [Related] [New Search]