1. Ouabain- and bumetanide-resistant (OBR) Na+ efflux from human erythrocytes into a Mg2+-sucrose medium exhibits kinetic properties consistent with a transmembrane Na+ leak.

2. In 52 essential hypertensive patients, the rate constant of Na+ leak (ke) was 15.0 ± 2.9 × 10−3h−1 (mean ±sd). This was significantly higher than the ke in 47 normotensive controls (13.2 ± 1.6 × 10−3h−1; t = 3.81, P < 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 bi-modally distributed. Nevertheless, if the upper end of the normotensive population is used as a cutoff point, it appears that a subgroup of 12 hypertensive patients had an increased Na+ leak, ke = 19.5 ± 1.9 × 10−3 h−1 (mean±sd). The increased Na+ leak remained constant in repeated determinations over several months.

3. 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.

4. 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.

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