An inherited sodium ion-potassium ion cotransport defect in essential hypertension.

1. In erythrocytes, the extrusion of a cell sodium load is accomplished by the ouabain-sensitive sodium-potassium pump and by the frusemide-sensitive sodium-potassium cotransport, which operate against the passive sodium permeability. All these three components of the cell sodium balance were studied in essential hypertension (410 subjects were investigated). 2. An abnormally low rate of net sodium extrusion by the sodium-potassium cotransport system was observed in essential hypertensive patients and in a high proportion 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. 3. A 20-40% increase in the rate of net sodium extrusion by the sodium-potassium pump seems to compensate for the abnormal cotransport in erythrocytes from some young normotensive subjects born of essential hypertensive parents and from some benign essential hypertensive subjects. 4. No difference could be detected between the passive sodium permeability of erythrocytes from hypertensive subjects and in those from normotensive controls. 5. In conclusion, essential hypertension seems to be associated with an inherited defect in the sodium-potassium cotransport system. We propose therefore the laboratory study of this system for: (i) the distinction between essential and secondary hypertension and (ii) the preventive investigation of young normotensive subjects in hypertensive families.