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

Aly M. Abdelrahman, Eef Harmsen, Frans H.H. Leenen

Research output: Contribution to journalArticle

12 Citations (Scopus)

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 [γ-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 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 (α1 and α2) in several areas of the brain and one binding site in the kidneys (α1) 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.

Original languageEnglish
Article number00006
Pages (from-to)517-522
Number of pages6
JournalJournal of Hypertension
Volume13
Issue number5
Publication statusPublished - 1995

Fingerprint

Dietary Sodium
Inbred Dahl Rats
Salts
Sodium
Diet
Hypothalamus
Kidney
Brain
Pons
Protein Isoforms
Binding Sites
Immunoglobulin Fragments
Immunoglobulin Fab Fragments
Ouabain
Microsomes
sodium-translocating ATPase
Sodium Chloride
Adenosine Triphosphatases
Arterial Pressure
Hydrolysis

Keywords

  • Brain
  • Digibind
  • Hypertension
  • Isoform
  • K-ATPase
  • Kidney
  • Na
  • Sodium

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Dietary sodium and Na,k-ATPase activity in Dahl salt-sensitive versus salt-resistant rats. / Abdelrahman, Aly M.; Harmsen, Eef; Leenen, Frans H.H.

In: Journal of Hypertension, Vol. 13, No. 5, 00006, 1995, p. 517-522.

Research output: Contribution to journalArticle

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AU - Leenen, Frans H.H.

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N2 - 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 [γ-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 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 (α1 and α2) in several areas of the brain and one binding site in the kidneys (α1) 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.

AB - 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 [γ-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 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 (α1 and α2) in several areas of the brain and one binding site in the kidneys (α1) 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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