[Role of microcirculation in hypertension].
A large share of the pressure gradient in the vascular system is situated in the microcirculation. Most of the mechanisms resulting in an increase of peripheral resistances during hypertension are also located in this network. Experimental studies have shown that the functional characteristics of arterioles are profoundly modified in most hypertension models. The sensitivity to vasoconstrictor agonists is increased. The activity of the angiotensin-converting enzyme, situated in the arteriolar wall, is considerably greater in genetically hypertensive animals than in control animals. Endothelium-dependent vasodilator mechanisms are also decreased in these animals, while endothelium-derived vasoconstrictor factors are responsible for an increased smooth muscle response. These functional disorders are associated with structural modifications of the microvascular network. Changes of wall thickness are observed only inconstantly, but an initially functional then anatomical rarefaction of arterioles and capillaries has been observed in most experimental models of hypertension and in several clinical studies. This phenomenon reduces the capacities of adaptation of perfusion condition to changes in metabolic requirements of the various organs, reflecting the fact that the microcirculation is a target of hypertensive disease. Antihypertensive drugs should therefore be assessed not only in terms of the reduction of blood pressure figures, but also in terms of their capacity to prevent or correct structural changes of the microvascular network.
Vicaut
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Laboratoire d'étude de la microcirculation, Hôpital François Widal, 200, rue du Faubourg Saint-Denis, 75010 Paris, France.
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001160:Arterioles / Q000503:physiopathology; D001794:Blood Pressure; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D008833:Microcirculation / Q000503:physiopathology*; D012084:Renin-Angiotensin System; D012212:Rheology; D014655:Vascular Resistance
D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents