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

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Abstract
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 Na balance. To investigate this further, Na transport and intracellular electrolyte composition was studied 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 2 extremes of Na balance, Na loading caused a nonsignificant rise in Na transport, whereas Na depletion was associated with a significant fall in Na transport and intracellular Na. When cells from salt-loaded or normal animals were incubated in a medium containing their own serum Na transport was slightly stimulated in both, but there was no significant difference in the Na 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 Na efflux-rate constant in any of the hypertensive rat models studied. However, the Na efflux-rate constant fell with age in both the spontaneously hypertensive and Wistar-Kyoto normotensive rats. Dietary Na intake and aging apparently had considerable effects on rat thymocyte Na transport, but neither of these changes was related to a change in blood pressure. Moreover, the raised blood pressure that developed in genetic, renovascular and mineralocorticoid hypertension was not associated with a significant change in Na transport. The currently described changes in membrane electrolyte transport of cells not directly involved in blood pressure control, in association with hypertension, probably reflect a fundamental change in the cell membrane. This change may not necessarily be related to the raised blood pressure. Further, Na depletion, rather than Na loading, produces inhibition of active Na pumping in this cell.