Davidge S T, McLaughlin M K
Department of Pediatrics, University of Cincinnati College of Medicine, OH.
Am J Obstet Gynecol. 1992 Dec;167(6):1691-8. doi: 10.1016/0002-9378(92)91763-z.
We tested the hypothesis that during pregnancy the endothelium mediates the blunted response to adrenergic vasoconstriction.
Mesenteric resistance arteries from late pregnant (n = 6) and age-matched virgin control (n = 6) Sprague-Dawley rats were studied in a myograph.
Arteries from pregnant rats were 35% less sensitive to phenylephrine vasoconstriction than were those from nonpregnant rats (mean effective concentration that produced a 50% response 2.26 vs 1.48 mumol/L, pregnant vs nonpregnant, p < 0.01). Meclofenamate had no effect on the vasoconstrictor response in arteries from either group. Inhibition of endothelium-derived relaxing factor with N(o)-nitro-L-arginine methyl ester or endothelial cell removal had a similar twofold increase in phenylephrine sensitivity in arteries from both the pregnant and nonpregnant rats (mean effective concentration that produced a 50% response 2.26 vs 1.11 mumol/L for pregnant rats and 1.48 vs 0.72 mumol/L for nonpregnant rats, p < 0.01). However, methacholine relaxation response was potentiated in pregnant versus nonpregnant rats (mean effective concentration that produced a 50% response 0.030 vs 0.049 mumol/L, p < 0.01).
Although the potential for endothelium-dependent relaxation is augmented in mesenteric arteries of the pregnant rat, the decreased sensitivity to phenylephrine during pregnancy is not modulated acutely by endothelium-derived relaxing factor or by prostaglandin products of the cyclooxygenase pathway.