Dietary sodium and Na,K-ATPase activity in Dahl salt-sensitive versus salt-resistant rats.

OBJECTIVE

To investigate the effects of high dietary sodium on brain and kidney Na,K-ATPase activity in Dahl salt-sensitive (Dahl-S) and salt-resistant (Dahl-R) rats.

METHODS

From the age of 4 weeks Dahl-S and Dahl-R rats were fed either standard or high-sodium diet (8% sodium chloride) for 3 weeks. The hydrolysis of [gamma-32P]-ATP in the absence or presence of various concentrations of ouabain was used to determine apparent Na,K-ATPase activity and its isoform composition. To assess whether reduced Na,K-ATPase activity and its isoform composition. To assess whether reduced Na,K-ATPase activity was caused by an endogenous inhibitor, brain and kidney microsomes were pre-incubated with antibody Fab fragments (Digibind).

RESULTS

The high-sodium diet increased mean arterial pressure in the Dahl-S but not in the Dahl-R rats. Two binding sites (alpha 1 and alpha 2) in several areas of the brain and one binding site in the kidneys (alpha 1) were detected. The high-sodium diet reduced Na,K-ATPase activity in the hypothalamus of the Dahl-S but not of the Dahl-R rats, but did not cause changes in the brain cortex, pons or kidney. The Na,K-ATPase isoform composition in the brain cortex, hypothalamus and pons and kidney was not changed by the high-sodium diet. In the rats fed the standard-sodium diet, Digibind increased Na,K-ATPase activity only in the hypothalamus of the Dahl-S rats. In rats fed the high-sodium diet, Na,K-ATPase activity was increased by Digibind in the hypothalamus of both strains of rats, but by more in the Dahl-S rats.

CONCLUSION

The present data indicate that a high-sodium diet inhibits hypothalamic Na,K-ATPase via increased binding of an inhibitor.