Preeclampsia is featured by increases in systolic and diastolic blood pressures, often followed by proteinuria after the 20th gestational week. Theories suggest that preeclampsia may be caused by poor placentation and that this diminishes the elasticity of the maternal-fetal interface vessels, impairing blood flow to the uterus and that may cause placental hypoperfusion and ischemia, which releases vasoactive factors into maternal circulation, resulting primarily in endothelial dysfunction. The main objective of the present study is to evaluate the repercussions on the cardiovascular system of offspring in an experimental model of gestational hypertension in rats. Pregnant rats will be allocated into two groups: Group 1 will be normotensive pregnant rats and Group 2 will be hypertensive pregnant rats. Gestational hypertension will be induced by deoxycorticosterone acetate and replacement of drinking water by saline. We will perform hemodynamic assessment by measuring the blood pressure and monitoring of the heart rate in mothers and first-generation offspring male rats. First-generation offspring male rats will be allocated into two groups: Group 3 will be male rats descending from normotensive pregnant rats and Group 4 will be male rats descending from hypertensive pregnant rats. At 90 days old, offspring male rats will be killed and the thoracic aorta will be removed and used in vascular reactivity experiments. We will investigate the impact of gestational hypertension on the offspring's cardiovascular system by assessing the hemodynamic parameters mentioned above and also the vascular contractility to phenylephrine and endothelium-dependent vasodilation. Therefore, our hypothesis is that there may be negative cardiovascular repercussions on the offspring male rats from hypertensive pregnant rats (model). We will also determine the concentrations of nitric oxide metabolites.
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