Correlation between Blood Pressure and K + Fluxes in Essential Hypertensive Patients Treated For 2 Years with Cicletanine

Essential hypertension appears to result from a combination of genetic and environmental factors, of which an excess Na+ intake is the most important (1). In the past ten years, the extensive investigation of Na+ transport in erythrocytes from essential hypertensive patients revealed at least four different and stable Na+ transport abnormalities (for details see ref. 2, 3, 4): (i) [Leak (+)] = increased passive entry of Na+ in about 15 to 30% of human hypertensives (Leak (+) hypertensives). (ii) [Co (-)] = decreased ability of the furosemide-sensitive Na+, K+ cotransport system to extrude a cell Na+-load in about 30 to 40% of human hypertensives (Co (-) hypertensives). (iii) [Counter (+)] = increased maximal rate of Na+: Li+ countertransport in about 20 to 40% of human hypertensives (Counter (+) hypertensives). (iv) [Pump (-)] = decreased apparent affinity of the Na+, K+ pump for internal Na+ in about 5–10% of human hypertensives.