SUMMARY We studied erythrocyte cation cotransport and countertransport systems in 21 and 27 patients with essential hypertension, respectively, all of whom were under 50 years of age, had a diastolic blood pressure level greater than 100 mm Hg, and had a family history of hypertension. The following parameters were normal in nearly all patients: total erythrocyte Na + and K + concentrations, the maximal rate (Vmax) of inward cotransport, the affinity of cotransport with Rb + as the substrate, the net outward cotransport of Na + ions, the passive "leak" influx of Rb, + and the maximal rate of Li + -Na + countertransport. Only four patients gave clearly abnormal results; in two the maximal rate of both cotransport and countertransport was double the normal values, while another two patients demonstrated a greater than twofold increase in passive "leak" influx to Rb + ions. Most of the patients with moderate to severe essential hypertension in this Australian study were characterized by normal erythrocyte cation fluxes, but a few showed elevation of both cotransport and countertransport of cations. (Hypertension 6: 360-368, 1984) KEY WORDS • essential hypertension countertransport erythrocyte cation transport • cotransport F OUR components of Na + transport have been characterized in human erythrocytes, three of which are facilitated by membrane carriers. The first of these three is an active cation pump identified with membrane (Na + + K + )-stimulated adenosine triphosphatase (ATPase) that extrudes Na + from the cell and is inhibited by ouabain.1 The second is a passive cotransport of (Na + + K + ) ions that mediates an equimolar flux of both ions across the membrane by a bidirectional mechanism. This transport system is inhibited by the loop diuretics furosemide and bumetanide.2 The third is Na + -Na + exchange diffusion, which occurs by a mechanism that also mediates the countertransport of Li + for Na + ions. 3 Finally, Na + ions may cross the membrane by a simple passive leak, the magnitude of which is directly proportional to the concentration gradient for this cation. An increase in the maximal rate of Li + -Na + countertransport has been demonstrated in erythrocytes from patients with essential hypertension both in studies
Extracellular Mg2+ is known to inhibit the passive Na+ and K+ fluxes in the human erythrocyte. In this study the effect of extracellular Mg2+ on Li+ efflux was measured in erythrocytes from 29 normotensive and essential hypertensive subjects. Magnesium produced a variable inhibition of between 0 and 47% in Li+ efflux in different subjects and this effect was unrelated to initial cell Li+, blood pressure or to an action on the co- or counter-transport pathways for this cation. A positive correlation was observed between the magnitude of the passive Li+ efflux and its inhibition (0 to 47%) by Mg2+ ions. Thus Mg2+ has an inhibitory effect on passive Li+ permeability which is unrelated to essential hypertension.
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