Endothelial dysfunction in hypertension

Endothelial cells release both relaxing and contracting factors that modula te vascular smooth muscle tone and also participate in the pathophysiology of essential hypertension. Endothelium-dependent vasodilation is regulated primarily by nitric oxide b ut also by an unidentified endothelium-derived hyperpolarizing factor and b y prostacyclin. Endothelium-derived contracting factors include endothelin- 1, vasoconscrictor prostanoids, angiotensin II and superoxide anions. Under physiological conditions, there is a balanced release of relaxing and cont racting factors. The balance can be altered in cardiovascular diseases such as hypertension, atherosclerosis, diabetes and other conditions, thereby contributing to fu rther progression of vascular and end-organ damage. In particular, endothel ial dysfunction leading to decreased bioavailability of nitric oxide impair s endothelium-dependent vasodilation in patients with essential hypertensio n and may also be a determinant for the premature development of atheroscle rosis. Different mechanisms of reduced nitric oxide activity have been shown both in hypertensive states and several cardiovascular diseases. and endothelial dysfunction is likely to occur prior to vascular dysfunction. Thus, the strategies currently used to improve endothelial dysfunction may result in decreased morbility and mortality in hypertensive patients.