The responses to endothelial vasodilators and exogenous nitric oxide (NO) were characterized in intact isolated uterine vascular beds of nonpregnant, midpregnant and late-pregnant rats perfused with Kreb's buffer (37 degrees C, 5% CO(2) in air, pH approximately 7.4) containing 2% dextran and indomethacin. Phenylephrine increased perfusion pressure in the vascular beds equally in all three groups. In the presence of phenylephrine, N(omega)-nitro-L-arginine methyl ester (L-NAME) significantly augmented perfusion pressure in the order: nonpregnant<midpregnant<late-pregnant uterine vascular bed. Acetylcholine and bradykinin-induced attenuation of perfusion pressure did not depend on gestational age. The decrease in perfusion pressure induced by acetylcholine was nonsignificantly attenuated by L-NAME in vascular beds from pregnant rats. The attenuation induced by bradykinin reached significant level in the vascular beds from midpregnant rats. The diethylamine (DEA)/NO-induced decrease in perfusion pressure was not influenced by L-NAME in any group. These data demonstrate the augmentation of basal release of NO associated with progression of pregnancy, while the responses to endothelial vasodilators do not depend on gestational age and are not abolished by inhibition of NO synthase, suggesting involvement of nonprostanoid non-NO factor in the control of uterine circulation.