Ki+-Nao+ countertransport in erythrocytes of patients with essential hypertension.
1. We describe in this paper a new ouabain-insensitive pathway for Na+ and K+ in human erythrocytes. K+ efflux was measured in cells loaded by the p-chloromercuribenzene-sulphonate (PCMBS) procedure to contain approximately equal amounts of Na+ and K+. K+ efflux was stimulated by external Na+ in the presence of ouabain and frusemide. Na+-stimulated K+ efflux was 0.35 +/- 0.12 (mmol h-1 l-1 of cells) in eight normal subjects and 0.64 +/- 0.13 in 13 patients with essential hypertension. 2. The Na+-stimulated K+ efflux was not observed in cells loaded in the presence of EGTA. This inhibition by EGTA suggests that K+ efflux is dependent on intracellular calcium. The Ki+-Nao+ countertransport of hypertensive patients was also inhibited by EGTA. The elevated K+-Na+ countertransport of hypertensive patients could be due to a higher intracellular Ca2+ content (Ca2i+) or to an increased affinity for Cai2+. The relationship of this pathway to the Gardos effect is not clear since Na+-stimulated K+ efflux occurs without metabolic depletion or inhibition of the Ca2+ pump. As a tentative hypothesis, we relate the Ca2+-dependent downhill movement of K+ and Na+ to the Ca2+-dependent channels described in muscle and nerve, but other hypotheses cannot be excluded at this stage of our research.
D002463:Cell Membrane Permeability; D004912:Erythrocytes / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000097:blood*; D007473:Ion Channels / Q000378:metabolism; D011188:Potassium / Q000097:blood*; D012964:Sodium / Q000097:blood*
D007473:Ion Channels; D012964:Sodium; D011188:Potassium