In vitro vascular reactivity of the rat utero-feto-placental unit.

Abstract

To evaluate the vascular reactivity to vasoconstrictor drugs and the local role of angiotensin I-converting enzyme in the rat utero-feto-placental unit. The experiments were carried out in vitro on a new model of the isolated perfused uterine horn from 19 nonpregnant and 16 pregnant rats. Norepinephrine, angiotensin II, and angiotensin I induced concentration-dependent vasoconstriction in non-pregnant uteri (50% effective concentration = 271 +/- 63, 9.9 +/- 3.7, and 1.7 +/- 0.8 x 10(-9) mol/L, respectively; n = 4-5, mean +/- standard error of the mean). In pregnant uteri, the maximum vasoconstrictor effects of norepinephrine (increase in perfusion pressure 132 +/- 6 versus 186 +/- 20 mmHg in pregnant and nonpregnant, respectively) and angiotensin II (37 +/- 9 versus 89 +/- 4 mmHg), but not angiotensin I, were significantly lower. The vasoconstrictor effect of angiotensin I was inhibited by saralasin, an antagonist of the angiotensin II receptors, and by ramiprilat, a converting-enzyme inhibitor. The isolated perfused rat utero-feto-placental unit is a useful experimental model for studying uterine vascular reactivity during pregnancy. Our in vitro results confirm vascular refractoriness to norepinephrine and angiotensin II during pregnancy and demonstrate local angiotensin II synthesis in the rat uterine vascular bed.