K_i⁺-Na⁺_o 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 K_i⁺-Na_o⁺ 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 (Ca_i²⁺) or to an increased affinity for Ca_i²⁺. 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.