Genetic variation in erythrocyte membrane ion transport and possible relationship to essential hypertension

Serial experiments were performed in order to understand and explore the Na+ transport system. In order to test possible covariation of cation and anion permeabilities, we applied inhibitors of cation or anion transport. Sulfonamide loop diuretics, furosemide and bumetanide, suppress 22/sub Na+/ influx into high permeability (HP) red cells but less into low permeability (LP) erythrocytes. These drugs also inhibit SO4 = transport about 70% in both types of RBC. RBC pretreated with impermeant polyanions also show significantly decreased Na+ influx into HP but not LP RBC. However,a potent inhibitor of RBC anion transport, diisothiocyanostilbene disulfonate (DIDS), has no influence on Na+ transport. Since the glucose channel is another transmembrane protein in erythrocyte membranes, the effects of the potent glucose transport inhibitors, phlorizin and phloretinyl-3'-benzylazide (PBAz), were measured. Both chemicals effect reduction of Na+ flux. Because radioactive PBAz is not available, we employed another potent Na+ channel blocker, 32P-8-azido-ATP, in an attempt to label HP and LP RBC membranes. Autoradiograms showed that 32P labels only band 4.2 and external iodination with 125I yields similar results