Mechanism of the interaction of hypertension and hypercholesterolemia in atherogenesis: the effects of antihypertensive agents.

Any alteration in the balance between serum lipids, platelets, hemodynamic factors, and the blood vessel wall may lead to the development of atherosclerosis. Hypertension and hypercholesterolemia are two major risk factors that accelerate the development of coronary heart disease. The mechanisms of the interactions of these two risk factors are examined in this paper. First, hypertension may be associated with focal or generalized endothelial injury or dysfunction. The altered endothelial functional integrity may predispose to platelet aggregation and altered vessel wall interaction, which may stimulate proliferation and growth of vascular cells. Second, elevated serum cholesterol levels may accelerate lipid deposition and formation of atherosclerotic plaques. In hypertension the rate of clearance of lipoprotein from the vessel wall may be reduced. Third, the sympathetic nervous system may be involved in both the development of hypertension and the alterations of lipid metabolism. Adrenergic activation, which increases blood pressure may also adversely affect lipid metabolism. This is in part alpha 1-adrenoceptor mediated. Selective alpha 1-inhibitors have been found to prevent or reduce atherosclerosis in experimental animals. Selective alpha 1-inhibitors may act at a number of sites on lipoprotein metabolic pathways to favorably influence serum lipids. Taken together, the relationship between hypertension and atherosclerosis involves complex mechanisms. A complete understanding of the mechanisms is of obvious importance.