Cell membrane handling of sodium, sodium balance, and blood pressure

A variety of abnormalities in cell membrane cation handling have been reported in hypertension. It is not known whether abnormal transport serves as a marker of an underlying disturbance in cell membrane function or whether one or more of the abnormal transport processes participate directly in the sequence of events that cause hypertension. One critical area is the response of membrane sodium transport to salt depletion and loading. To elucidate a possible relationship between changes in sodium balance, membrane cation transport, and blood pressure, we studied the effect of salt depletion and loading in two cells from two separate species--the rat thymocyte and the human white blood cell. In each, severe salt depletion significantly reduced ouabain-sensitive sodium efflux, while salt loading produced a non-significant increase. No significant changes in the sodium efflux rate constant were observed in thymocytes from Okamoto-Kyoto spontaneously hypertensive rats or from rats with Goldblatt one-kidney, one-clip or deoxycorticosterone-salt hypertension when they were compared with appropriate controls. However, both Okamoto-Kyoto hypertensive rats and Kyoto controls showed a highly significant fall in the sodium efflux rate constant with age. These findings indicate that the reduction in sodium pumping observed in hypertensive human patients is not attributable directly or indirectly to salt excess, since in the two species studied reduced sodium pumping was a physiological response to salt depletion. Further, altered membrane transport of sodium may reflect factors that affect cell composition (such as age) rather than participate directly in the pathogenesis of hypertension.