Estrogen-induced uterine vasodilatation is antagonized by L-nitroarginine methyl ester, an inhibitor of nitric oxide synthesis

Am J Obstet Gynecol. 1992 Sep;167(3):828-33. doi: 10.1016/s0002-9378(11)91597-x.

Abstract

Objectives: Our study was designed to determine whether nitric oxide mediates estrogen-induced increases in uterine blood flow.

Study design: Six nonpregnant oophorectomized ewes were instrumented with uterine artery flow probes and catheters. Ewes received estradiol-17 beta 1 microgram/kg, which maximally increased uterine blood flow by 120 minutes. Each animal then received local bolus injections of the nitric oxide synthetase inhibitor L-nitroarginine methyl ester.

Results: Estradiol-17 beta increased uterine blood flow from 16 +/- 6 to 139 +/- 32 ml/min by 120 minutes. Local uterine artery administration of L-nitroarginine methyl ester (1 to 30 mg) caused a dose-related decrease in uterine blood flow, which reached a maximum of 59% +/- 6% inhibition. Higher doses of L-nitroarginine methyl ester less than or equal to 10 mg/kg (330 to 460 mg) given locally led to a maximum inhibition of 79% +/- 3% but showed systemic responses.

Conclusion: Estradiol-17 beta-induced increases in uterine blood flow are mediated mainly by nitric oxide; the observed vasodilation can be antagonized by the intraaterial administration of nitric oxide synthetase inhibitor L-nitroarginine methyl ester.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Arginine / analogs & derivatives*
  • Arginine / pharmacology
  • Dose-Response Relationship, Drug
  • Estradiol / pharmacology*
  • Female
  • NG-Nitroarginine Methyl Ester
  • Nitric Oxide / antagonists & inhibitors*
  • Nitric Oxide / metabolism
  • Regional Blood Flow / drug effects
  • Sheep / blood
  • Uterus / physiology*
  • Vasodilation / drug effects*

Substances

  • Nitric Oxide
  • Estradiol
  • Arginine
  • NG-Nitroarginine Methyl Ester