OBJECTIVE: To test the hypothesis that vascular relaxation kinetics are pro
longed in pregnant rats treated chronically with N-omega-nitro-L-arginine m
ethyl ester (L-NAME).
METHODS: Timed pregnant rats (on day 15 of a 22-day gestation) were implant
ed with infusion pumps containing vehicle (controls) or L-NAME (50 mg/d). L
-NAME pumps were retained were mounted in organ chambers containing physiol
ogic salt solution (PSS) for isometric tension recording, contracted with h
igh-K+ PSS (60 mM), and allowed to relax in normal-K+ PSS. Relaxation kinet
ics were qualified as time for 50% and 80% relaxation. After contraction wi
th phenylephrine, responses to cumulative concentrations of methacholine we
re studied in the absence and presence of L-arginine (L-Arg) (10(-3) M).
RESULTS: Responses to methacholine were inhibited completely in group 1 and
partially in group 2 (P < .05). The inhibition in both groups was reversed
by L-Arg. The rate of relaxation was significantly slower in groups 1 and
2 (P < .05), but not in group 1. Preincubation of aortic rings from untreat
ed controls with L-NAME (in vitro, 10(-4) M) did not affect relaxation.
CONCLUSION: The endothelium modulates the rate of vascular relaxation by a
factor other than nitric oxide. N-omega-nitro-L-arginine methyl ester (L-NA
ME) prolongs vasorelaxation by endothelium-dependent and -independent mecha
nisms. Prolongation of vascular relaxation kinetics may be a mechanism to e
levate blood pressure and peripheral vascular resistance in preeclampsia. C
opyright (C) 1999 by the Society for Gynecologic Investigation.