Nitric Oxide Blunts Sympathetic Response of Pregnant Normotensive and Hypertensive Rat Arteries

Abstract

Abstract Rat pregnancy is associated with a blunted response to vasocontrictors both in vivo and in vitro as well as a decrease in arterial pressure. We examined the influence of pregnancy on neurally induced vasoconstrictor and vasodilator responses of the isolated mesenteric arterial bed from normotensive Wistar and spontaneously hypertensive nonpregnant and 20-day pregnant rats and determined the possible role of nitric oxide (NO) in modulating these responses. MAP (mm Hg) in pregnant normotensive (98±1, n=13) and hypertensive (136±5, n=13) rats was lower ( P <.05) than in nonpregnant controls (114±2, n=14, and 174±3, n=12, respectively). In isolated mesenteric arterial beds, electrical field stimulation (EFS; 34 V, 3 ms, 10-64 Hz) of perivascular nerves at basal tone induced a frequency-dependent increase in perfusion pressure that was significantly ( P <.001) greater in preparations from hypertensive compared with normotensive rats. Pregnancy was associated with a significant decrease in the maximal vasoconstrictor response elicited by EFS in both normotensive and hypertensive groups compared with their nonpregnant controls. In phenylephrine-preconstricted mesenteric beds, EFS (60 V, 1 ms, 1-8 Hz) elicited a similar frequency-dependent decrease in perfusion pressure in normotensive and hypertensive groups, but pregnancy did not influence these responses. In the presence of the NO synthase inhibitor N ω -nitro- l -arginine (200 μmol/L), the maximal vasoconstrictor response induced by EFS was significantly ( P <.001) augmented in both normotensive and hypertensive groups, and the differences observed between pregnant and nonpregnant groups were abolished. Responses to sodium nitroprusside were not affected by pregnancy, although they were greater in preparations from hypertensive rats. These results indicate that NO contributes to pregnancy-associated diminished vasoconstrictor response to sympathetic stimulation in the mesenteric arterial bed of both normotensive and hypertensive rats.