Erythrocytic sodium ion transport systems in primary and secondary hypertension of the rat.

Sodium and potassium ion transport systems were studied in erythrocytes from spontaneously hypertensive Okamoto rats (SHR), hypertension-prone Sabra rats (SbH), and one-kidney one-clip Goldblatt hypertensive rats, and compared with Wistar-Kyoto normotensive rats (WKY), hypertension-resistant Sabra rats (SbN), and sham-operated Wistar rats. We observed the following: (1) An increased net potassium influx and a reduced net sodium extrusion occurred in SHR. The increased potassium influx was inhibited by ouabain, indicating an increased sodium ion pump activity. Bumetanide-sensitive sodium extrusion was lower in SHR than it was in WKY, indicating abnormally low outward sodium-potassium cotransport fluxes. (2) Passive sodium ion permeability was increased in SbH compared with SbN. Cotransport was normal in SbH rats. (3) Sodium-potassium cotransport and passive permeability were normal in renovascular hypertension. (4) After a chronic or acute sodium load, the sodium content increased in erythrocytes from SHR and SbH but not in those of normotensive or renal hypertensive rats. It appears therefore that erythrocyte membrane abnormalities leading to an increased intracellular sodium concentration are only present in genetic hypertension. The reduction of outward sodium-potassium cotransport observed in SHR is identical to that previously reported in human essential hypertension, suggesting that it may be considered as a genetic marker.