IN-VITRO VASCULAR REACTIVITY OF THE RAT UTERO-FETO-PLACENTAL UNIT

Objective: To evaluate the vascular reactivity to vasoconstrictor drug s and the local role of angiotensin I-converting enzyme in the rat ute ro-feto-placental unit. Methods: The experiments were carried out in v itro on a new model of the isolated perfused uterine horn from 19 nonp regnant and 16 pregnant rats. Results: Norepinephrine, angiotensin II, and angiotensin I induced concentration-dependent vasoconstriction in nonpregnant 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 +/- s tandard error of the mean). In pregnant uteri, the maximum vasoconstri ctor effects of norepinephrine (increase in perfusion pressure 132 +/- 6 versus 186 +/- 20 mmHg in pregnant and nonpregnant, respectively) a nd angiotensin II (37 +/- 9 versus 89 +/- 4 mmHg), but not angiotensin I, were significantly lower. The vasoconstrictor eff ect of angiotens in I was inhibited by saralasin, an antagonist of the angiotensin II r eceptors, and by ramiprilat, a converting-enzyme inhibitor. Conclusion : The isolated perfused rat utero-feto-placental unit is a useful expe rimental model for studying uterine vascular reactivity during pregnan cy. Our in vitro results confirm vascular refractoriness to norepineph rine and angiotensin II during pregnancy and demonstrate local angiote nsin II synthesis in the rat uterine vascular bed.