In this study, we investigated smooth muscle cell contractions induced by angiotensin II (ANG II) in blood vessels with or without endothelium after ischemia/reperfusion. Experiments were done on tail arteries, with or without endothelium, of perfused male Wistar rats. We analyzed the influence of ANG II on vascular contractions in the presence of sodium nitroprusside or 8Br-cGMP and after ischemia/reperfusion using classical pharmacometric methods. Vascular contractions induced by ANG II were decreased by sodium nitroprusside and 8BrcGMP. Reductions in maximal response and increases in $EC_{50}$ values after ischemia were observed only in vessels with endothelium. After reperfusion, increases in maximal response and decreases in $EC_{50}$ values were observed. Decreases in ANG II induced vascular contractions on caused by ischemia involves the presence of endothelium, synthesis of nitric oxide and activation of cGMP. The increase in the reaction to ANG II that is induced by reperfusion is independent of the endothelium.