title: Platelet and erythrocyte Mg2+, Ca2+, Na+, K+ and cell membrane adenosine triphosphatase activity in essential hypertension in blacks.
abstract: OBJECTIVE
  To assess the relationship between intracellular Mg2+, Ca2+, Na+ and K+ and cell membrane adenosine triphosphatase (ATPase) activity in normotensive and hypertensive blacks.
  
  
  METHODS
  Intracellular cations and cell membrane ATPase activity were studied in black patients with untreated essential hypertension and age-, weight- and height-matched normotensive controls. Platelet, erythrocyte and serum Mg2+, Ca2+, Na+ and K+ levels as well as platelet and erythrocyte membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase activities were measured in all subjects.
  
  
  METHODS
  Intracellular Na+ and K+ were measured by flame photometry and Mg+ and Ca+ by atomic absorption spectrophotometry. Cell membrane ATPase activity was determined by a colorimetric method.
  
  
  RESULTS
  The hypertensive group consistently demonstrated depressed activity of each ATPase studied, with significantly lower serum Mg2+, serum K+, erythrocyte Mg2+ and platelet Mg2+ levels compared with the normotensive group. Platelet Na+ and Ca2+ and erythrocyte Ca2+ were significantly elevated in the hypertensive group. In the hypertensive group, mean arterial pressure (MAP) was inversely correlated with platelet and erythrocyte membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase. Serum Mg2+, serum Ca2+ and platelet Mg2+ were negatively correlated with MAP in the hypertensive group whilst erythrocyte and platelet Ca2+ were positively correlated. In the normotensive group, platelet Mg2+ and MAP were negatively, and erythrocyte Ca2+ and MAP, positively correlated.
  
  
  CONCLUSIONS
  Black patients with essential hypertension have widespread depression of cell membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase activities with serum and intracellular Mg2+ depletion and cytosolic Na+ and Ca2+ overload, which may reflect an underlying membrane abnormality in essential hypertension. These cellular abnormalities may be related to the defective transport mechanisms that in turn may be aggravated by Mg2+ depletion.
authors.affiliation: Department of Medicine, University of Witwatersrand Medical School, Johannesburg, South Africa.
authors.forename: R M
authors.initials: RM
authors.lastname: Touyz
authors.forename: F J
authors.initials: FJ
authors.lastname: Milne
authors.forename: S G
authors.initials: SG
authors.lastname: Reinach
mesh_terms: D044383:Black People; D001792:Blood Platelets / Q000737:chemistry / Q000201:enzymology*; D017301:Ca(2+) Mg(2+)-ATPase / Q000097:blood*; D000252:Calcium-Transporting ATPases / Q000097:blood*; D002458:Cell Fractionation / Q000379:methods; D002462:Cell Membrane / Q000737:chemistry / Q000201:enzymology; D004910:Erythrocyte Membrane / Q000737:chemistry / Q000201:enzymology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000201:enzymology*; D008297:Male; D012016:Reference Values; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood*; D013019:South Africa
chemical_list: D017301:Ca(2+) Mg(2+)-ATPase; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase