Ouabain-Sensitive and -Insensitive Cation Transport in in Normotensives and Hypertensives in Hypokalemic States

Abstract

Several years ago, it was reported that red blood cells of patients with essential hypertension contain an increased sodium concentration [1]. It could be demonstrated that the passive Na⁺ influx into these erythrocytes was augmented in contrast to other types of hypertension [2]. Recently, results of a new test have been published by Garay and Meyer [3] showing abnormal net Na⁺ and K⁺ fluxes in erythrocytes of essential hypertensive patients. In Na⁺-loaded/K⁺-depleted red cells of these patients, a constant increase in net K⁺ influx and a reduced ratio of Na⁺/K⁺ net fluxes were observed; this was not seen in hypertensives of renal origin. Wambach et al [4] reported an increased Na⁺/K⁺-ATPase activity in erythrocyte ghosts of patients with essential hypertension. In our earlier studies [5], we could not confirm these findings. We did, however, measure an increased number of ³H-ouabain binding sites and of Na⁺/K⁺-ATPase activity in erythrocytes of patients with hypokalemia due to chronic diuretic treatment. Canessa et al [6] reported an increased sodium-lithium countertransport in red cells of patients with essential hypertension, apparently without overlap with normotensive people.