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Enhanced volume-sensitive K flux in patients on chronic hemodialysis
Swelling-activated K flux was investigated in erythrocytes from patients on regular hemodialysis. K influx, measured by 86Rb uptake, was increased in hemodialysis patients from 25.5 +/- 0.6 to 47.3 +/- 3.4 nmol/10(9) cells/h (n = 4, p < 0.01), when the medium osmolarity of Hepes buffer was decreased by 100 mosm/kg H2O. In normal subjects, K influx was also stimulated from 28.1 +/- 1.2 to 37.8 +/- 2.1 nmol/10(9) cells/h (n = 4, p < 0.01). The swelling-activated increment of K influx was comparatively higher in hemodialysis patients (85.5 vs. 34.5% in controls). Reduction of the medium osmolarity by 100 mosm/kg H2O also caused a larger increase of K efflux in hemodialysis patients than in control subjects (171.1 vs. 118.1%). K efflux was increased even in the presence of 10(-4) M ouabain (from 284 +/- 25 to 879 +/- 122 nmol/10(9) cells/h), although the increment of K efflux was completely abolished when Cl was replaced by gluconate (555 +/- 47 nmol/10(9) cells/h with Cl and 467 +/- 44 nmol/10(9) cells/h without Cl). These data suggest that in hemodialysis patients, swelling-activated K transport is enhanced via activation of the Cl-dependent ouabain-insensitive K transport pathway.
Swelling-activated K flux was investigated in erythrocytes from patients on regular hemodialysis. K influx, measured by 86Rb uptake, was increased in hemodialysis patients from 25.5 +/- 0.6 to 47.3 +/- 3.4 nmol/10(9) cells/h (n = 4, p < 0.01), when the medium osmolarity of Hepes buffer was decreased by 100 mosm/kg H2O. In normal subjects, K influx was also stimulated from 28.1 +/- 1.2 to 37.8 +/- 2.1 nmol/10(9) cells/h (n = 4, p < 0.01). The swelling-activated increment of K influx was comparatively higher in hemodialysis patients (85.5 vs. 34.5% in controls). Reduction of the medium osmolarity by 100 mosm/kg H2O also caused a larger increase of K efflux in hemodialysis patients than in control subjects (171.1 vs. 118.1%). K efflux was increased even in the presence of 10(-4) M ouabain (from 284 +/- 25 to 879 +/- 122 nmol/10(9) cells/h), although the increment of K efflux was completely abolished when Cl was replaced by gluconate (555 +/- 47 nmol/10(9) cells/h with Cl and 467 +/- 44 nmol/10(9) cells/h without Cl). These data suggest that in hemodialysis patients, swelling-activated K transport is enhanced via activation of the Cl-dependent ouabain-insensitive K transport pathway.