Uterine arterial responses to arachidonate in pregnant and nonpregnant rabbits.

Abstract

Several investigators have suggested that prostaglandins (PG) may play a major regulatory role in maintaining uteroplacental blood flow in pregnancy. The present study was undertaken to assess the response of the uterine artery from near-term pregnant and nonpregnant rabbits to the PG precursor Na-arachidonate (AA) (C 20:4). Isolated uterine arterial strips were equilibrated isometrically under their optimal resting tensions in physiologic salt solution. Uterine arteries from pregnant rabbits elicited significantly greater contractile responses to arachidonate over the dose-range studied (10(-10)-10(-3) M) than did arteries from nonpregnant rabbits. These contractions were seen whether the strip was relaxed or precontracted with potassium chloride (30 mM). The contractile responses to AA were antagonized in a competitive manner by pretreating the arteries with the cyclooxygenase inhibitors meclofenamate (10(-5) M) or indomethacin (10(-5) M), thus suggesting that the contractile response to AA was the result of its conversion to prostanoids by the cyclooxygenase pathway. The possibility that the AA response was a general fatty acid effect was ruled out since oleate (C 18:1) had no effect on the arteries. In addition, prostaglandins F2 alpha and E2 (10(-5) M) also contracted the uterine arteries from the pregnant group. It is concluded from these studies that the uterine arterial wall from near-term pregnant rabbits utilizes the PG precursor, AA, for the production of prostanoids which, in turn, cause uterine arterial constriction.