Increased sodium-lithium countertransport in red cells of patients with essential hypertension.

This paper describes experiments showing that one of the pathways of sodium transport across the red-cell membrane, sodium-lithium countertransport, is faster in patients with essential hypertension than in control subjects. This transport system accepts only sodium or lithium and is not inhibited by ouabain. The maximum rate of transport shows inherited differences. The mean maximum rate of sodium-lithium countertransport was found to be 0.55 +/- 0.02 (mean +/- S.E.M.) mmol (liter of red cells X hour)(-1) in a group of 36 patients with essential hypertension and 0.24 +/- 0.02 in 26 control subjects (P less than 0.001). The first-degree relatives of eight patients with essential hypertension and 10 control subjects had mean maximum rates of sodium-lithium countertransport of 0.54 +/- 0.05 and 0.23 +/- 0.02, respectively. Five patients with secondary hypertension had normal mean maximum rates of sodium-lithium countertransport. The relation between heritability of red-cell sodium-lithium countertransport and essential hypertension should be investigated further.

[1]  R. Garay,et al.  A NEW TEST SHOWING ABNORMAL NET Na+ AND K+ FLUXES IN ERYTHROCYTES OF ESSENTIAL HYPERTENSIVE PATIENTS , 1979, The Lancet.

[2]  D. Tosteson,et al.  Kinetics and stoichiometry of Na-dependent Li transport in human red blood cells , 1978, The Journal of general physiology.

[3]  J. R. Sachs.  Ouabain-Insensitive Sodium Movements in the Human Red Blood Cell , 1971, The Journal of general physiology.

[4]  D. Tosteson,et al.  Coupling of lithium to sodium transport in human red cells , 1975, Nature.

[5]  D. Tosteson,et al.  Effects of bicarbonate on lithium transport in human red cells , 1978, The Journal of general physiology.

[6]  D. Phear.  Salt Intake and Hypertension , 1958, British medical journal.

[7]  D. Tosteson,et al.  Abnormal lithium and sodium transport in erythrocytes of a manic patient and some members of his family. , 1977, Proceedings of the National Academy of Sciences of the United States of America.

[8]  D. Tosteson,et al.  A heritable disorder of lithium transport in erythrocytes of a subpopulation of manic-depressive patients. , 1978, The American journal of psychiatry.

[9]  J. Mendels,et al.  Genetic determinant of lithium ion distribution. I. An in vitro monozygotic-dizygotic twin study. , 1974, Archives of general psychiatry.

[10]  F. Kregenow,et al.  THE CHARACTERIZATION OF NEW ENERGY DEPENDENT CATION TRANSPORT PROCESSES IN RED BLOOD CELLS , 1966, Annals of the New York Academy of Sciences.

[11]  W G ZIJLSTRA,et al.  Standardization of hemoglobinometry. II. The hemiglobincyanide method. , 1961, Clinica chimica acta; international journal of clinical chemistry.

[12]  D. Tosteson,et al.  Lithium transport in human red blood cells: genetic and clinical aspects. , 1979, Archives of general psychiatry.

[13]  R. A. Cooper,et al.  A furosemide-sensitive cotransport of sodium plus potassium in the human red cell. , 1974, The Journal of clinical investigation.

[14]  D. Tosteson,et al.  Lithium transport pathways in human red blood cells , 1978, The Journal of general physiology.

[15]  I. Glynn,et al.  The sodium pump. , 1975, Annual review of physiology.

[16]  L. Beaugé.  Non-pumped sodium fluxes in human red blood cells. Evidence for facilitated diffusion. , 1975, Biochimica et biophysica acta.