INCREASED REACTIVITY OF RAT UTERINE ARCUATE ARTERY THROUGHOUT GESTATION AND POSTPARTUM

Significant modifications of the uterine circulation are observed duri ng pregnancy, with uterine circulation accounting for up to 11% of car diac output at the end of pregnancy. We studied the reactivity of the uterine microcirculation to determine the time course of uterine mecha nical and pharmacological alterations during pregnancy and postpartum. Arcuate artery segments, obtained from virgin, pregnant (7, 14, and 2 2-23 days), and postpartum (5 days) rats, were set up in wire myograph s for microvessels under a passive tension equivalent to a transmural pressure of 50 mmHg (L-50). Cumulative concentration-response curves t o angiotensin II (ANG II), phenylephrine (PE), and potassium chloride (KCl) were measured. Diameter of the arcuate artery at L-50 increased progressively until term from 108 +/- 4 mu m in virgins to 188 +/- 9 m u m at day 22 of pregnancy. This increase in diameter was partially re versed at day 5 postpartum (151 +/- 9 mu m) Surprisingly, the passive length-tension relationship on arcuate arteries showed greater stiffne ss from day 14 of pregnancy through day 5 postpartum. The maximum resp onse of the arteries to ANG II was markedly increased during pregnancy (from 0.78 +/- 0.02 to 1.43 +/- 0.09 mN/mm at day 22) and was already evident at day 14 (1.20 +/- 0.07 mN/mm) but was reversed in postpartu m rats (0.81 +/- 0.04 mN/mm, nonsignificant). Similar results were obt ained for maximum responses to PE and KCl, but the reversal at day 5 p ostpartum was only partial. Sensitivity (measured as the negative log of the concentration of stimulant required to produce 50% of the maxim um response) of the uterine arcuate artery to the three vasopressors i ncreased during the postpartum period and also at day 22 of pregnancy with PE and day 24 with KCl. The present results show that the uterine arcuate artery doubles in diameter during pregnancy. This increase in diameter is accompanied by increased stiffness of the vessel and heig htened responsiveness to ANG II, PE, and KCl. These data demonstrate t hat pregnancy induces changes in reactivity of the rat uterine arcuate artery that appear to be linked to modifications in the mechanical pr operties of the vessel, at least for ANG II and PE.