Estrogen and progesterone regulate alpha, beta, and gammaENaC subunit mRNA levels in female rat kidney.

No abstract is available for this paper.

• Publication year

  2004

• Venue

  Kidney International

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  PMID 15086916
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Renal inactivation, mineralocorticoid generation, and 11beta-hydroxysteroid dehydrogenase inhibition ameliorate the antimineralocorticoid effect of progesterone in vivo.

  2003cited by this paper
• The human kidney is a progesterone-metabolizing and androgen-producing organ.

  2003cited by this paper
• Endogenous and exogenous glucocorticoid regulation of ENaC mRNA expression in developing kidney and lung.

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  2002cited by this paper
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• The serum- and glucocorticoid-induced kinase is a physiological mediator of aldosterone action.

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• Chronic Exposure to Vasopressin Upregulates ENaC and Sodium Transport in the Rat Renal Collecting Duct and Lung

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• Inhibitory non-genomic effects of progesterone on Na+ absorption in epithelial cells from Xenopus kidney (A6)

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• Acute differential regulation by corticosteroids of epithelial sodium channel subunit and Nedd4 mRNA levels in the distal colon

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• Glucocorticoid Induction of Epithelial Sodium Channel Expression in Lung and Renal Epithelia Occurs via trans-Activation of a Hormone Response Element in the 5′-Flanking Region of the Human Epithelial Sodium Channel α Subunit Gene*

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• Aldosterone-mediated regulation of ENaC alpha, beta, and gamma subunit proteins in rat kidney.

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• Regulation of rENaC mRNA by dietary NaCl and steroids: organ, tissue, and steroid heterogeneity.

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• Regulation of stability and function of the epithelial Na+ channel (ENaC) by ubiquitination

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• Diversity of Channels Generated by Different Combinations of Epithelial Sodium Channel Subunits

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• Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1

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