Evidence against a circulating ouabain-like transport inhibitor as a cause of increased red cell sodium in essential hypertension.

Red cell sodium and potassium concentrations, and total ouabain-sensitive and ouabain-insensitive first order red constants for sodium efflux, were measured in 15 patients (11 female, 4 male) with essential hypertension (162 +/- 14/99 +/- 7 (s.d. mmHg) and 15 normotensive control subjects (117 +/- 17/64 +/- 10 mmHg) individually matched for age (45.8 +/- 10 versus 45.7 +/- 10 years, respectively, sex, weight (68.6 +/- 16.1 versus 64.7 +/- 11.2 kg) and blood group. To test for possible plasma inhibitors of sodium transport in hypertension, total efflux rate constants were measured in red cells incubated in two plasma samples, from either the same or the complementary (paired) subjects, respectively. Intracellular sodium was significantly increased in patients (11.8 +/- 3.45 versus 8.75 +/- 2.48 mmols/l of red cell water; P = 0.023). Intracellular potassium and total and ouabain-sensitive sodium efflux rate constants, were similar in both groups. Sodium efflux was similar when cells were incubated in the homologous and complementary plasma samples. Ouabain-insensitive rate constants were decreased in the patients (0.16 +/- 0.08 versus 0.20 +/- 0.05 h-1) but the difference was of borderline significance (P = 0.059). These results confirm the presence of abnormal intracellular sodium concentrations and membrane transport in essential hypertension but are not consistent with the suggestion that the abnormalities are due to a circulating sodium transport inhibitor.