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* * * * * * * * * * * * 吴春荣175 梁万年;专升本75 梁万年;专升本75 * * * * * * Hypertension and other CV risk factors (eg, diabetes, smoking, and dyslipidaemia) are associated with dysfunction of the vascular endothelium and remodelling of the vessel walls. This affects vascular function, aggravates increased BP levels, and accelerates the development of atherosclerosis.1,2 Background The normal vascular endothelium regulates many processes that are key for the maintenance of vascular structure and function, including vascular tone, growth, hemostasis, inflammation, and redox state. Endothelial dysfunction is involved in the vasomotor dysfunction of coronary arteries. The atherosclerotic process underlying the pathogenesis of CAD results in limited ability to supply oxygen on demand and affects the normal vasodilatation/vasoconstriction process in coronary arteries and microcirculation.1 Excessive production of oxygen free radicals and subsequent metabolism of nitric oxide (NO) results in oxidative stress. The imbalance between the activities of nitric oxide (NO) and angiotensin-II causes oxidative stress and dysfunction of the vascular endothelium associated with the pathogenesis of atherosclerosis.1 Overproduction of oxygen free radicals counteracts the effects of NO and stimulates the expression of adhesion molecules, which facilitates the attachment of leukocytes to the vascular endothelium. This process results in acute inflammatory response, proliferation of smooth muscle cells, and synthesis of extracellular matrix molecules, all of which contribute to the development of CVD.1 References 1. Pepine CJ. The effects of angiotensin converting enzyme inhibition on endothelial dysfunction: potential role in myocardial infarction. Am J Cardiol. 1998;82(suppl 10A):23S-27S. 2. Schiffrin EL; Canadian Institutes of Health Research Multidisciplinary Research Group on Hypertension. Beyond blood pressure: the endothelium and atherosclerosis progression. Am J Hypertens. 2002;15:115s-1
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