A PROPOSED GENETIC MARKER OF ESSENTIAL HYPERTENSION

In erythrocytes, the e xtrusion of a cell sodium load is accompl ished by the ouabain-sensiti ve sodiurn-potassium pump and by the furosemide-sensitive sodium-potassium cotransport, which operate against the passive sodium permeability. The precise characteri zation of these transport pathways requires the determination of the turnover r ates of cation translocation and the affinities for subtrates and effectors. The preliminary results of such kinetic study in essential hypertension is reported here. An abnormally low rate of net sodium extrusion by the sodiumpotassium co-transport system was observed in essential hypertensive patients and in a high p roportion of their young normotensive offspring. A normal cotransport system found in secondary hypertensive subjects devoid of familial history of hypertension confirmed that the abnormal cotransport system is not the consequence of high blood pressure per se. At the molecular level, the cotransport abnormality seems to be consecutive to a diminished apparent affinity for intracellular Nat.