[New data on mineralocorticoid hormones. Physiopathological implications]

Our better understanding of the terminal steps of aldosterone production based on enzyme cloning has led to new clinical approaches to three aldosterone-related types of hypertension: mineralocorticoid excess, Liddle's disease and glucocorticoid-sensitive hyperaldosteronism. In all three cases, hypertension results from volume expansion due to increased reabsorption of sodium in the distal renal tube with decreased plasma renin activity and hypokaliaemia. Genetic testing now allows early diagnosis of these severe familial diseases and specific treatment. Although both glucocorticoid-sensitive hypertension and Liddle's disease are dominantly inherited diseases, other genes can also modulate the degree of volume expansion, hypokaliaemia and blood pressure levels within a given family. The degree of hypertension observed in a given individual results from the interactions between the expression of "hypertenser" and "hypotenser" genes. Recent progress raises the possibility that other similar genetic mechanisms exist in more common forms of primary hypertension. Systematic exploration of the renin-angiotensin-aldosterone system based on measurement of the renin/aldosterone ratio as proposed in the diagnosis of primary hyperaldosteronism will make it possible to determine whether there exists a relationship between these genes and the hypertension observed.