[ATPase activity and sodium transport in erythrocytes of patients with essential hypertension (author's transl)].

The rate constant for erythrocyte "total" sodium efflux was significantly decreased in patients with essential hypertension compared with normotensive controls due to a reduced "ouabain-sensitive" (active) sodium transport. The rate constants for "ouabain-insensitive", "ouabain-insensitive furosemide-sensitive" and "ouabain-insensitive furosemide-insensitive" sodium efflux were not different between hypertensives and normotensives. Ouabain inhibited sodium efflux by 74% and furosemide by a further 13%, both in hypertensives and in normotensives. The reduced rate constant for active erythrocyte transport in patients with essential hypertension was due to a diminished Na-K-ATPase activity demonstrable in hemolyzed and dialyzed erythrocytes. In contrast, in hemoglobin-free red blood cell membranes Na-K-ATPase activity was not different between both groups. Apparently the centrifugation procedure, which is necessary for preparation of hemoglobin-free membranes, leads to a loss of non-hemoglobin proteins, including ouabain-sensitive and ouabain-insensitive ATPase and/or a Na-K-ATPase inhibiting factor. Thus, the results obtained in hemolyzed and dialyzed red blood cells reflect probably better the conditions in the intact erythrocyte than do measurements on hemoglobin-free membranes, suggesting a decreased Na-K-ATPase activity in erythrocytes of essential hypertensives. However, the diminished rate constant for ouabain-sensitive sodium efflux did not result in a measurable increase in erythrocyte sodium indicating that this biochemical abnormality can fully be compensated in moderate essential hypertension without excess salt intake. The cause of the reduced rate constant for ouabain-sensitive sodium efflux is not clear. However, as suggested for sodium-potassium cotransport and for sodium-lithium countertransport it might be determined genetically.