[Endothelium and hypertension].
Many changes in endothelial function have been described in hypertension. Endothelium-dependant dilatation due to the stimulation of specific receptors or related to changes in flow, are reduced both in experimental models and in clinical observations of hypertensive patients. Many mechanisms of this endothelial dysfunction have been proposed. Reduction of the activity of the enzyme synthesising nitric oxide has been found in some animal modes of hypertension (salt-related) and in hypertensive subjects whereas in other experimental models, this enzyme's activity is increased. Other mechanisms, therefore, play a role, such as increased synthesis of constricting prostanoids and increased synthesis of oxygen radicals. The inhibition of cyclooxygenase or intra-arterial administration of Vitamin C in hypertensive patients may restore endothelium-dependant vasodilatation. In view of the many endothelium-dependant mechanisms described in the pathogenesis of hypertension, the authors underline the fact that in most studies each mechanism has been studied individually. However, understanding the interactions of the different endothelial dependant mechanisms is the key to reconciling the many physiopathological disturbances observed in hypertension, differentiating direct from indirect changes induced by the complex network of interactions one with another. This will also result in a more accurate appreciation of the similarities and differences of effects of antihypertensive drug therapy targeted on endothelial function.
Vicaut
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Laboratoire d'étude de la microcirculation, hôpital Fernand-Widal, 20, rue du Faubourg-Saint-Denis, 75010 Paris.
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology; D004195:Disease Models, Animal; D004727:Endothelium / Q000473:pathology* / Q000502:physiology; D005609:Free Radicals; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D014664:Vasodilation
D005609:Free Radicals; D019001:Nitric Oxide Synthase; D001205:Ascorbic Acid