title: [Essential arterial hypertension, cellular intolerance to sodium].
abstract: Much experimental and clinical evidence points to the fact that increased intracellular Na+ concentration could play an important pathogenic role in hypertension, especially where cells of excitable tissues are concerned. Active extrusion of Na+ (from the cells to the extracellular space) depends mainly on the activity of the system of membrane transport known as the Na+ pump. The extrusion of Na+ occurs in exchange for K+ and the activity of the pump depends on the enzyme Na+-K+-ATPase. The Na+ pump is inhibited by cardiotonic glycosides such as digitalis and ouabain . The results obtained in our laboratory suggest that the activity of the Na+ pump is controlled by an endogenic system acting in a similar manner to ouabain and digitalis. Experimental and clinical studies show: -- that the administration of Na+ increases the inhibitor effect both in urine and plasma; -- that the inhibitor is increased in about 50 p. 100 of patients with essential hypertension; -- that this increase seems to depend on familial or genetic factors. The biochemical identification of this endogenic inhibitor is now under way; it has a small molecular weight (less than 3000), is thermostable and anionic. This factor could have both a regulating role on Na+ turnover and a pathological role in hypertension. Its activity comes into competition cations also capable of inhibiting the Na+ pump, including K+.
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D055598:Chemical Phenomena; D002621:Chemistry; D004285:Dogs; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007473:Ion Channels / Q000378:metabolism; D045283:Natriuretic Agents; D011188:Potassium / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism*
chemical_list: D007473:Ion Channels; D045283:Natriuretic Agents; D011506:Proteins; D012964:Sodium; D011188:Potassium
vernacular_title: L'hypertension artérielle essentielle, une intolérance cellulaire au sodium.