Abstract :
[en] Established essential HTA is considered to result from the influence of both heredity and environment. Among the environmental factors, dietetary sodium has been proposed to play an important role inducing an increase in peripheral vascular resistance. The primary abnormality
in essential HTA could consist in a genetically transmitted membrane defect impairing the cellular mechanisms which normally compensate a sodium load. The analysis of this defect implies more certainly elucidation of the effects of sodium ions at the blood vessel musculature level. But smooth muscle cells are unfortunately rather inaccessible. Yet it would be of great interest to dispose of a simple laboratory test to detect primary HTA. Therefore, on account of their availability and ease of manipulation, blood cells have been studied and already twenty years ago, LOSSE (12) recorded an increase of the intracellular sodium concentration in erythrocytes of
hypertensive patients. Since then, different groups described different abnormalities' in the movement of ions across the blood cells membranes. Indeed modifications of the passive permeability (11, 12, 13), the sodium potassium pump (1, 5, 14), the sodium lithium countertransport (2, 7, 18) and the sodium potassium cotransport (3, 8, 9,10) have been successively demonstrated. GARAY et al. (9,10,11) observed a decrease in this last transport system for essential hypertensives and a high proportion of their young offspring. Conversely for normotensive patients, without a family history of HTA or in secondary hypertensives, a normal cotransport was found. The finding of an abnormal cotransport in a young normotensive may thus elicit preventive measures such as appropriate sodium diet, prevention of excessive weight gain, clinical follow up during oral contraception or pregnancy. The first observations showed a very clearcut difference between the two populations. However, many authors using the same test procedure, found a large overlap suggesting the measurement of this cotransport will not prove useful to discriminate primary HTA. However, the methodology was not always the same and difference could also arise from the definition of normal control groups which needed to be carefully selected. Thus in this study, we would evaluate the modification of the Na+ K+ cotransport in primary and secondary HTA, using strictly the experimental methodology originally described by GARAY et al. (9, 10). Afterwards, it would be interesting to study the effect of obesity, diabetes and the menstrual cycles on this transport system.
