Erythrocyte sodium and sodium flux in relation to hypertension in chronic renal failure.
Erythrocyte sodium and sodium fluxes in plasma and in physiological buffer solution were studied in normotensive and hypertensive uraemic patients and normal subjects. Erythrocyte sodium was reduced in the uraemic patients due primarily to low sodium influx, further supported by low passive membrane permeability. These differences were much more marked in normotensive patients. There was no evidence for sodium pump inhibition in the erythrocytes. The low erythrocyte sodium influx in the uraemic patients appeared to be due to a plasma factor which could be reversed in young cells but not in old. However, erythrocyte sodium flux in both plasma and physiological buffer was lower in normotensive than in hypertensive uraemic patients. Therefore, a membrane change to compensate for the effects of the plasma factor on sodium influx may be related to the development of hypertension in the uraemic patients.
Thomas
T H
TH
Department of Medicine, University of Newcastle upon Tyne, UK.
Mansy
H
H
Wilkinson
R
R
D000328:Adult; D002478:Cells, Cultured; D004905:Erythrocyte Aging / Q000187:drug effects; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000097:blood*; D007676:Kidney Failure, Chronic / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood*; D015222:Sodium Channels / Q000378:metabolism*
D015222:Sodium Channels; D010042:Ouabain; D005665:Furosemide; D012964:Sodium; D011188:Potassium