NITRIC-OXIDE BLUNTS SYMPATHETIC RESPONSE OF PREGNANT NORMOTENSIVE ANDHYPERTENSIVE RAT ARTERIES

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 vasoconstr ictor and vasodilator responses of the isolated mesenteric arterial be d from normotensive Wistar and spontaneously hypertensive nonpregnant and 20-day pregnant rats and determined the possible role of nitric ox ide (NO) in modulating these responses. MAP (mm Hg) in pregnant normot ensive (98 +/- 1, n = 3) 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 perivasc ular nerves at basal tone induced a frequency-dependent increase in pe rfusion pressure that was significantly (P < .001) greater in preparat ions 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-preconstric ted mesenteric beds, EFS (60 V, 1 ms, 1-8 Hz) elicited a similar frequ ency-dependent decrease in perfusion pressure in normotensive and hype rtensive groups, but pregnancy did not influence these responses. In t he presence of the NO synthase inhibitor N-omega-nitro-L-arginine (200 mu mol/L), the maximal vasoconstrictor response induced by EFS was si gnificantly (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 aff ected by pregnancy, although they were greater in preparations from hy pertensive rats. These results indicate that NO contributes to pregnan cy-associated diminished vasoconstrictor response to sympathetic stimu lation in the mesenteric arterial bed of both normotensive and hyperte nsive rats.