Sodium transport across the red cell membrane and pathogenesis of essential hypertension: perspectives.
The possible roles of an acceleration of Na+-Li+ exchange and an alteration of Na+-K+ cotransport in the pathogenesis of hypertension are ascertained. Evidence is presented to indicate that the red cell Na+-Li+ exchange activity is goverened not only by genetic factors but also by plasma constituents that can vary in vivo. Of particular importance are the plasma K+ concentration and the plasma lipid composition. Red cell Na+-Li+ exchange activities increase with increasing saturation of the fatty acids in the membrane. An unifying hypothesis is proposed linking the primary change in plasma lipids to a secondary change of the lipid composition of cell membranes, resulting in alterations of lipo-protein interactions within the membrane and thereby in alterations of Na+ (and Ca2+) transport in several tissues, including erythrocytes. Such a mechanism could be responsible for development of high blood pressure in a subgroup of essential hypertensive patients that is characterized by a specific alteration in plasma lipid composition the precise nature of which remains to be investigated.
D000818:Animals; D017920:Antiporters; D001692:Biological Transport; D001696:Biomechanical Phenomena; D002352:Carrier Proteins / Q000502:physiology; D002417:Cattle; D004910:Erythrocyte Membrane / Q000378:metabolism*; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D012964:Sodium / Q000097:blood* / Q000378:metabolism; D028021:Sodium-Potassium-Chloride Symporters
D017920:Antiporters; D002352:Carrier Proteins; D028021:Sodium-Potassium-Chloride Symporters; C045885:sodium-lithium countertransporter; D012964:Sodium