Alterations in sodium metabolism as an etiological model for hypertension.
An adequate matching for race, sex, stage of the menstrual cycle, family history of hypertension, and the amount of sodium and other electrolytes in the diet should be a prerequisite for valid conclusions when interpreting the erythrocyte concentration and fluxes of sodium in essential hypertensive patients in comparison with normal subjects. Alterations in intracellular sodium concentration and transmembrane sodium transport systems as causes of essential hypertension are postulated. This review article describes how this abnormal sodium and calcium metabolism translates into increased systemic vascular resistance through altered vasoactive responses and/or vasculature structural changes.
Department of Molecular and Cardiovascular Research, University of Leuven, Belgium.
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D017920:Antiporters / Q000378:metabolism* / Q000502:physiology; D001639:Bicarbonates / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D004912:Erythrocytes / Q000166:cytology / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D017136:Ion Transport; D008094:Lithium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism* / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology
D017920:Antiporters; D001639:Bicarbonates; D002712:Chlorides; D017923:Sodium-Hydrogen Exchangers; C045885:sodium-lithium countertransporter; D008094:Lithium; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium