title: Membrane transport, sodium balance, and blood pressure regulation.
abstract: Essential hypertension is characterized by polygenic inheritance and quantitative and/or qualitative abnormalities of membrane transport systems may function as intermediate phaenotypes. The present review attempts to evaluate the importance of sodium transport systems such as the sodium pump, cotransport and countertransport as aetiological or pathogenetic factors involved in primary hypertension. Furthermore, the relative importance of NaCl balance as an exogenous factor modifying these transport systems is reviewed. Controversial results exist with respect to the activity of the sodium pump and cotransport both as a function of blood pressure and NaCl balance. In contrast, accumulating evidence suggests that the activity of the counter-transport system is increased in essential hypertension and that this may be observed even before the elevation of blood pressure can be documented. In own studies performed in normotensive volunteers on a low (20 mmol/day) and high (320 mmol/day) NaCl intake, lymphocyte antiport activity was significantly higher during chronic NaCl loading. Therefore, alterations of the Na+/H+ antiport system may represent an intermediate phaenotype of gene(s) involved in the genesis of primary hypertension. Preliminary evidence suggests that NaCl balance may be an exogenous modulator of this system.
authors.affiliation: Medizinische Universitäts-Poliklinik Bonn, FRG.
authors.forename: B O
authors.initials: BO
authors.lastname: Göbel
authors.forename: G
authors.initials: G
authors.lastname: Hoffmann
authors.forename: M
authors.initials: M
authors.lastname: Ruppert
authors.forename: K O
authors.initials: KO
authors.lastname: Stumpe
authors.forename: H
authors.initials: H
authors.lastname: Vetter
authors.forename: R
authors.initials: R
authors.lastname: Düsing
mesh_terms: D000818:Animals; D001692:Biological Transport; D001794:Blood Pressure; D002712:Chlorides / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase
chemical_list: D002712:Chlorides; D012965:Sodium Chloride; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase