Effect Of Losartan On Expression Of ICAM-1 And PAI-1 On Aortic Intima Of Spontaneously Hypertensive Rats

Essential hypertension (EH) is the major risk factor of severity and coronary heart disease, but the mechanisms that cause essential hypertension occurring and developing has not been clarified. Recently many investigation data suggested that the alteration of adhesion between leuocyte and endothelial cell or fibriolytic system is one of the possible mechanisms and increase the incidence of thrombogenic complication. So, the selection of antihypertension drugs which could relieve the adhesion of cells and ameliorate the disturbance of fibriolytic system has significant clinical value. This study explored the effects of Losartan, an AngII type 1 (ATj) receptor antagonist, on the expression of intercellular adhesion molecule-1 (1CAM-1) and plasminogen activitor inhibitor-l(PAI-l) on aortic intima of early Spontaneously Hypertensive rats(SHR).Twenty SHR were divided randomizedly into 2 groups of 10 rats each. One group were fed with Losartan of 20mg/kg/d per day for 8 weeks,while the remained group (SHR control group) and 10 Wistar Kyoto rats(WKY) were given normol water only for equal time. Blood pressure of each rat was measured before and during the treatment. The expressions of ICAM-1 and PAI-1 on aortic intima of three groups rats were studied by immunohistochemistery. It was shown that the expression of ICAM-1 and of PAI-1 on aortic intima of SHR control group were higher than WKY group. It was shown markly lower expressions in Losartan group than that in SHR control group, and the blood pressure were decreased significantly. .The data suggested that : (1) the reinforcement of intercellular adhesion between leuocyte and endothelial cell and the alteration of fibriolytic system may be one of the mechanisms which cause EH. (2) ATiR could decrease the blood pressure of SHR significantly. (3) ATiR could relieve the adhesion of ceils and ameliorate the disturbance of fibriolytic system, which may control EH and prevent the occurring of thrombogenic complication.