Calcium binding capacity of erythrocyte membrane in human hypertension

The cell membrane calcium binding capacity of genetically hypertensive rats is reduced when measured in the presence of the submicromolar calcium concentrations proper of intracellular environment. The present work, performed as an ancillary study to an epidemiological survey on an entire population, aimed to investigate the existence of a similar abnormality in human hypertension. Calcium binding to the erythrocyte membrane was measured in clinically healthy normotensive (n = 12) and hypertensive individuals (n = 24). For this purpose, a filtration technique was used, based on the determination of ⁴⁵Ca bound to the erythrocyte membrane in the presence of free calcium concentrations (40 nmol/l and 1 μmol/l), which are similar to those of the intracellular environment. The intra-assay technical error was determined on 35 duplicate samples and, when expressed as percent of the mean, was 24.1 at the 40 nmol/l concentration and 16.8 at the 1 μmol/l concentration. Membranes of untreated hypertensive patients, at both calcium concentrations, bound significantly less calcium than the control group. Treated and untreated hypertensive individuals had comparable values of membrane calcium binding capacity. Membranes of the treated hypertensive group bound less calcium than those of the normotensive group at both calcium concentrations, but the difference was statistically significant only in the presence of 40 nmol/l free calcium. A significant positive correlation was observed between the calcium binding capacity at 40 nmol/l concentration and that at 1 μmol/l in the treated and untreated hypertensive groups (r = 0.73 and 0.75, respectively; 0.51 for he normotensive group). These findings support the hypothesis that a cell membrane abnormality is detectable in some hypertensive patients. The possible pathophysiological meaning of the reduction in membrane calcium binding and its possible relation with the other disorders of cellular and systemic calcium homeostasis observed in hypertension need to be further investigated.