Na+ leak in erythrocytes from essential hypertensive patients.

Ouabain- and bumetanide-resistant (OBR) Na+ efflux from human erythrocytes into a Mg2+-sucrose medium exhibits kinetic properties consistent with a transmembrane Na+ leak. In 52 essential hypertensive patients, the rate constant of Na+ leak (ke) was 15.0 +/- 2.9 X 10(-3) h-1 (mean +/- SD). This was significantly higher than the ke in 47 normotensive controls (13.2 +/- 1.6 X 10(-3) h-1; t = 3.81, P less than 0.001; Mann-Whitney U rank sum test P = 0.0014). The relatively small number of patients studied was insufficient to decide if the hypertensive population was bimodally distributed. Nevertheless, if the upper end of the normotensive population is used as a cut-off point, it appears that a subgroup of 12 hypertensive patients had an increased Na+ leak, ke = 19.5 +/- 1.9 X 10(-3) h-1 (mean +/- SD). The increased Na+ leak remained constant in repeated determinations over several months. Na+ movements catalysed by the Na+-K+ co-transport and Na+-Li+ countertransport systems were measured in the above 52 hypertensive patients. Seventeen hypertensive patients showed a low apparent affinity of the co-transport system for internal Na+ and 12 exhibited a high maximal rate of Na+-Li+ countertransport. None of these two abnormalities was found in the 12 hypertensive patients with increased ke. We propose to denote them as Leak-(+) hypertensive patients. Passive net Na+ entry was abnormally high in all Leak-(+) hypertensive patients. However, erythrocyte Na+ content was increased in only five of the 12 Leak-(+) hypertensive patients. A normal or even decreased Na+ content was associated with the presence of compensatory increases in the maximal rate of the Na+-K+ pump and the Na+-K+ co-transport system.