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• W2080661917 abstract "Endothelin-1 (ET-1) is a potent and long-acting vasoactive peptide often implicated in the pathogenesis of hypertension. However, little is known about its role in the pathogenesis of hypertensive vascular disease. This study compares the vascular changes produced in vivo by pressor or subpressor doses of ET-1 and angiotensin II (ANG II) in rat intestinal arterioles. In one experiment, equivalent pressor doses of either ET-1 (0.2 μg/kg/min) or ANG II (2 μg/kg/min) were given. In a second experiment, subpressor doses of ET-1 (10 ng/kg/min) were either infused alone or given in combination with pressor doses of ANG II (2 μg/kg/min). Normal saline infusions (0.02 mL/min) served as controls. All infusions were continued for 60 minutes, interrupted for 30 minutes, and reinstituted for 30 minutes. Changes in vascular permeability were assessed using ferritin as a tracer; vascular lesions were assessed by computerized morphometry and electron microscopy. Results from the first experiment showed that ET-1 and ANG II produced approximately equivalent increases in blood pressure but that ET-1 had more prolonged pressor effects when infusions were interrupted. Pressor doses of either ET-1 or ANG II caused a segmental pattern of vasoconstriction and dilatation, an increase in ferritin permeability, and severe vascular smooth muscle damage. However, vessels from ET-1-treated animals had fewer damaged smooth muscle cells (p < 0.05) and smaller areas of vessel wall damage (p < 0.05) than did those from the ANG II-treated group. Subpressor doses of ET-1 in the second experiment produced no vascular lesions, but combined subpressor ET-1/pressor ANG II infusion caused greater hypertension (p < 0.05) and more extensive damage (p < 0.01) to greater numbers of vascular smooth muscle cells (p < 0.01) than did pressor infusions of ET-1 or ANG II alone. The results indicate that subpressor concentrations of ET-1 clearly potentiate the vascular damage caused by ANG II-induced hypertension. On the other hand, pressor doses of ET-1 do not cause more severe vascular injury than do equipresor doses of ANG II, though the hypertension induced by ET-1 has longer-lasting hypertensive effects." @default.
• W2080661917 created "2016-06-24" @default.
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• W2080661917 date "1993-10-01" @default.
• W2080661917 modified "2023-09-23" @default.
• W2080661917 title "Potential role of endothelin-1 in the pathogenesis of acute hypertensive vascular disease in the rat" @default.
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• W2080661917 doi "https://doi.org/10.1016/1054-8807(93)90035-z" @default.
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