Effects of changes in dietary sodium intake on aortic sodium pump activity in the rat.

Aortic smooth muscle sodium efflux was studied in normal rats undergoing salt restriction or salt loading. Sodium efflux rate constant was not changed by salt loading but fell significantly with salt restriction. This change was not associated with a fall in blood pressure. These studies show that smooth muscle sodium transport can be influenced by dietary salt intake but do not support the concept that salt loading leads to the inhibition of the vascular smooth muscle sodium pump.

Rat thymocyte sodium transport. Effects of changes in sodium balance and experimental hypertension.

The wide range of membrane electrolyte transport abnormalities associated with experimental, genetic, and essential hypertension may either reflect an underlying global change in the cell membrane or may be directly related to the underlying disturbance that causes hypertension or to changes in sodium balance. To investigate this further, we studied sodium transport and intracellular electrolyte composition in the thymocytes of normal rats undergoing salt loading or depletion, and in rats with renovascular, mineralocorticoid, or spontaneous hypertension compared to appropriate age-matched normotensive control rats. In normotensive rats, although there was no significant difference between the blood pressures at the two extremes of sodium balance, sodium loading caused a nonsignificant rise in sodium transport, whereas sodium depletion was associated with a significant fall in sodium transport and intracellular sodium. When cells from salt-loaded or normal animals were incubated in a medium containing their own serum, sodium transport was slightly stimulated in both, but there was no significant difference in the sodium efflux-rate constant of thymocytes obtained from rats on the normal as opposed to the high salt intake. Compared to normotensive rats, there was no significant change in the sodium efflux-rate constant in any of the hypertensive rat models studied. However, the sodium efflux-rate constant fell with age in both the spontaneously hypertensive and Wistar-Kyoto normotensive rats. The present studies show that dietary sodium intake and aging had considerable effects on rat thymocyte sodium transport, but neither of these changes was related to a change in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

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.