Endothelial dysfunction: its role in hypertensive coronary disease

Purpose of review Coronary artery disease is the major cause of death worldwide. Hypertension is a major risk factor for developing coronary disease. It is now recognized that enclothelial dysfunction is an early marker of coronary artery disease before structural changes to the vessel wall are apparent on angiography or intravascular ultrasound and that it has a prognostic value in predicting cardiovascular events in hypertensive patients. This review addresses recent developments in hypertension-induced enclothelial dysfunction. Recent findings Hyperalclosteronism causes enclothelial dysfunction independent of high blood pressure. Exaggerated exercise blood pressure response has been related to enclothelial dysfunction. Cyclosporin-A-induced enclothelial dysfunction is related to reduced cholesterol content in caveolae. Chronic kidney disease induces changes in caveoli-1 and thus contributes to the reduced nitric oxide bioavailability, and causes oxidative stress independent of the high blood pressure. Asymmetric dimethylarginine plays a role in enclothelial dysfunction in hypertensive patients independent of insulin resistance. 20-Hydroxyeicosatetraenoic acid is an independent predictor of hypertension in postmenopausal women. Endothelial dysfunction precedes and predicts the development of hypertension in postmenopausal women. Oral treatment with L-arginine improves enclothelial dysfunction in hypertensives and lowers the blood pressure. Summary The pathophysiology of enclothelial dysfunction in hypertension is multifactorial. Recent findings have contributed to our understanding of mechanisms of enclothelial dysfunction and support a role for early intervention to prevent irreversible vascular and organ damage.