Contraction and endothelium-dependent relaxation in mesenteric microvessels from pregnant rats

We assessed KCl- and phenylephrine (PE)-induced vasoconstriction as well as acetylcholine (ACh)-induced endothelium-dependent vasodilation in small, isometrically mounted mesenteric arteries from virgin and gravid rats, studied in the absence and presence of N-G-nitro-L-arginine (L-NNA). Neither maximal vasoconstriction nor PE potency differed significantly between vessels from virgin and pregnant rats, either in the absence or presence of L-NNA. L-NNA resulted in similar twofold leftward shifts in the PE dose-response curves for both groups. ACh-induced relaxation was potentiated in vessels from gravid rats (half-maximum effective concentration = 0.25 vs. 0.04 mu M, virgin and gravid rats, respectively). After L-NNA, maximal relaxation was inhibited significantly more in vessels from gravid rats (62 vs. 31%). Likewise, maximal slope of ACh dose-response curves and ACh potency were decreased in this group so that values no longer differed from those in virgins. We conclude that pregnancy does not alter basal nitric oxide (NO) synthesis in these isolated microvessels, but it does enhance ACh-induced NO release, while apparently inhibiting the action of a NO-independent, endothelium-derived vasodilator.