Impaired endothelial regulation of vascular tone in patients with systemic arterial hypertension.
The discovery of the endothelium as a major regulator of vascular tone triggered intense research among basic and clinical investigators to unravel the physiologic and pathophysiologic significance of this phenomenon. Importantly, endothelial modulation of the contractile state of vascular smooth muscle has been shown to be impaired in atherosclerosis and in several conditions known to be associated with the premature development of atherosclerosis. Studies in several different animal models of arterial hypertension, and in patients with both essential and secondary hypertension, have demonstrated an association between elevated systemic blood pressure and impaired endothelium-dependent vascular relaxation. More recently, a diminished bioavailability of nitric oxide (NO) has been identified as a mechanism responsible for endothelial dysfunction in hypertensive patients. Different processes may, in turn, explain this decreased vascular activity of NO. The present review focuses on those clinical studies that are aimed at identifying the precise abnormality responsible for reduced NO-dependent vasodilation in patients with essential hypertension. Understanding of the basic mechanisms of this process may prove to be beneficial for the development of more specific therapies and ultimately for the outcome of hypertensive patients.
Cardillo
C
C
Vascular Physiology Laboratory, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1650, USA.
Panza
J A
JA
D000818:Animals; D004730:Endothelium, Vascular / Q000502:physiology*; D004789:Enzyme Activation; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D009129:Muscle Tonus / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D013379:Substrate Specificity; D014666:Vasomotor System / Q000502:physiology*
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase