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Abdelrahman AM, Harmsen E, Leenen FH. Dietary sodium and Na,K-ATPase activity in Dahl salt-sensitive versus salt-resistant rats. J Hypertens. 1995;13(5):517-22doi: 10.1097/00004872-199505000-00006.
Abdelrahman, A. M., Harmsen, E., & Leenen, F. H. (1995). Dietary sodium and Na,K-ATPase activity in Dahl salt-sensitive versus salt-resistant rats. Journal of hypertension, 13(5), 517-22. https://doi.org/10.1097/00004872-199505000-00006
Abdelrahman, A M, et al. "Dietary sodium and Na,K-ATPase activity in Dahl salt-sensitive versus salt-resistant rats." Journal of hypertension vol. 13,5 (1995): 517-22. doi: https://doi.org/10.1097/00004872-199505000-00006
Abdelrahman AM, Harmsen E, Leenen FH. Dietary sodium and Na,K-ATPase activity in Dahl salt-sensitive versus salt-resistant rats. J Hypertens. 1995 May;13(5):517-22. doi: 10.1097/00004872-199505000-00006. PMID: 7561008.
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J Hypertens. 1995 May;13(5):517-22. doi: 10.1097/00004872-199505000-00006.

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

Journal of hypertension

A M Abdelrahman, E Harmsen, F H Leenen

Affiliations

  1. Hypertension Unit, University of Ottawa Heart Institute, Ontario, Canada.

PMID: 7561008 DOI: 10.1097/00004872-199505000-00006

Abstract

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.

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