title: Erythrocyte ion fluxes in essential hypertensive patients with left ventricular hypertrophy.
abstract: BACKGROUND
  Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular morbidity and mortality in essential hypertension (EH). Several hemodynamic and nonhemodynamic factors have been involved in the development of LVH in hypertension, including abnormalities in cellular ion mobilization.
  
  
  RESULTS
  We measured different ion transport systems in erythrocytes from 50 patients with EH classified as having or not having LVH measured by M-mode echocardiography. Thirty-two EH patients (64%) exhibited criteria of LVH, and 18 (36%) did not. When the two groups were compared, patients with LVH were older (44.7 +/- 7.4 versus 37.6 +/- 9.2 years; P < .01) and exhibited higher rates of erythrocyte Na(+)-H+ exchange (9.8 +/- 4.1 versus 7.1 +/- 2.6 mmol.[L.cells.h]-1; P < .05) and higher intraerythrocyte Na+ content (8.5 +/- 1.3 versus 7.5 +/- 0.8 mmol/L per cell; P < .01). Systolic and diastolic blood pressure values, as well as biochemical, hormonal, and other erythrocyte ion transport systems studied did not differ between EH with or without LVH. The results of a multiple linear regression analysis using left ventricular mass index (LVMI) as the dependent variable showed that Na(+)-H+ exchange and the maximal rate of the Na(+)-K(+)-Cl- cotransport were the only two independently significant parameters associated with an increased LVMI.
  
  
  CONCLUSIONS
  The increased rate of the erythrocyte Na(+)-H+ exchange and the decreased maximal rate of the Na(+)-K(+)-Cl- cotransport system are both associated with the presence of LVH in EH patients. These abnormalities of ion transport pathways tend to increase the intracellular Na+ content and may be involved in the pathogenesis of LVH in EH.
authors.affiliation: Department of General Internal Medicine, Hospital Clinico, School of Medicine, Barcelona, Spain.
authors.forename: A
authors.initials: A
authors.lastname: de la Sierra
authors.forename: A
authors.initials: A
authors.lastname: Coca
authors.forename: J C
authors.initials: JC
authors.lastname: Paré
authors.forename: M
authors.initials: M
authors.lastname: Sánchez
authors.forename: V
authors.initials: V
authors.lastname: Valls
authors.forename: A
authors.initials: A
authors.lastname: Urbano-Márquez
mesh_terms: D000328:Adult; D002352:Carrier Proteins / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000453:epidemiology / Q000209:etiology / Q000378:metabolism*; D017136:Ion Transport / Q000502:physiology; D008297:Male; D011188:Potassium / Q000378:metabolism; D011446:Prospective Studies; D012044:Regression Analysis; D012964:Sodium / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D028021:Sodium-Potassium-Chloride Symporters
chemical_list: D002352:Carrier Proteins; D002712:Chlorides; D017923:Sodium-Hydrogen Exchangers; D028021:Sodium-Potassium-Chloride Symporters; D012964:Sodium; D011188:Potassium