ROLE OF NITRIC-OXIDE AND CYCLOOXYGENASE PRODUCTS IN CONTROLLING VASCULAR TONE IN UTERINE MICROVESSELS OF RATS

The importance of nitric oxide (NO) and dilator prostaglandins in uter ine resistance arterioles was investigated. In pentobarbital anaesthet ized rats at dioestrus-2, the uterine microcirculation in vivo was tra nsilluminated by a fibreoptic probe and microvessels (circumferential arterioles) viewed by video microscopy. Arteriolar diameters were meas ured while increasing concentrations of acetylcholine (ACh), serotonin (5-HT), phenylephrine (PE), or angiotensin II (AII) were applied topi cally (suffused) over the uterus. Agonists were applied alone or with ibuprofen (IBU; cyclooxygenase inhibitor), N-omega-nitro-L-arginine (L -NA; nitric oxide synthase inhibitor) or both. Circumferential arterio les were dilated by ACh and 5-HT (10(-8)-10(-4)mol l(-1)) and constric ted by PE (10(-8)-10(-5) mol I-1) and AII (10(-11)-10(-7) mol l(-1)). Suffusion of L-NA or L-NA with ibuprofen (10(-4) mol l(-1) each) aboli shed ACh-induced dilation; ibuprofen alone blocked dilation at higher ACh concentrations. Serotonin-induced relaxation was significantly att enuated by L-NA alone or in combination with ibuprofen. Vasoconstricti on induced by PE was enhanced by L-NA alone and L-NA with ibuprofen, b ut ibuprofen alone had no effect. In contrast, AII-induced constrictio n was enhanced significantly by ibuprofen or L-NA and further enhanced when both ibuprofen and L-NA were present. These results suggest that ACh can release either nitric oxide (NO) or cyclooxygenase products t o cause uterine arteriolar dilation and that 5-HT-induced uterine micr ovascular relaxation is mediated via NO only. They also suggest that P E-induced vasoconstriction is attenuated by the release of NO but not cyclooxygenase products and that constrictor responses evoked by AII a re attenuated by both NO and dilator prostaglandin release. Thus, both nitric oxide and dilator prostaglandins are important in the control of uterine microvessels.