RESUMEN
Pregnancy is characterized by a blunted pressor response to angiotensin II that is progressively lost during preeclampsia complicated pregnancies. Renin angiotensin system (RAS) plays a pivotal role in cardiovascular and renal function but its role in normal and pathological pregnancy is far from being clarified. It is not as clear if hypertension and particularly pregnancy-induced hypertension as the initial event, can trigger some of the metabolic syndrome components, and if these changes are angiotensin II mediated. The aim of this study was to determine the time course of angiotensin II contribution to the vascular and eventual metabolic changes of preeclampsia. An experimental model was developed by reducing feto-placental circulation through a subrenal aorta coarctation before pregnancy in rats. Control and pregnant (preeclamptic) animals were treated with captopril (5mg/kgpo) or saline solution for 21, 14 or 7days before delivery, and their body weight, plasma glucose andblood pressure were registered. Phenylephrine (Phe) induced contraction was evaluated using isolated aorta rings. Preeclampsia increased blood pressure (2nd and 3rd wk) but also weight (3rd wk) and glucose values (2nd and 3rd week). Captopril (for 21 or 14days) treatment prevented increases in blood pressure and plasma glucose but not in body weight. Also, captopril treatment significantly increased aorta contractility. These results provide evidence that cardiovascular and metabolic disturbances of preeclampsia appear simultaneously and are angiotensin II dependent.