Localization of 11β-hydroxysteroid dehydrogenase: Specific protector of the mineralocorticoid receptor in mammalian olfactory mucosa

Robert C. Kern, Dimitri Z. Pitovski*

*Corresponding author for this work

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

The enzyme 11β-hydroxysteroid dehydrogenase (11βHSD) plays a major role in the protection of the mineralocorticoid (type 1) receptor. The cellular mechanism of aldosterone selectivity relies on the coexpression of mineralocorticoid receptors and 11βHSD in the same cells. In the current study, 11βHSD activity was localized in the mammalian olfactory mucosa by a histochemical technique which links steroid metabolism with the deposition of formazan. The histochemical reaction results from oxidation of the synthetic substrate 11β-hydroxyandrostenedione and is dependent on nicotine-adenine dinucleotide (NAD). This demonstrates the presence of a dehydrogenase activity separate from the nicotineamide-adenine dinucleotide phosphate (NADP)-dependent 11βHSD. In the olfactory mucosa, the presence of NAD- dependent 11βHSD activity is localized to the sustentacular cells and acinar cells of Bowman's glands. No definite NAD-dependent activity was demonstrated in the olfactory receptor neurons. These data suggest that mineralocorticoid receptors present in acinar cells and sustentacular cells are aldosterone selective.

Original languageEnglish (US)
Pages (from-to)738-743
Number of pages6
JournalActa Oto-Laryngologica
Volume117
Issue number5
DOIs
StatePublished - Jan 1 1997

Keywords

  • Bowman's gland
  • Glucocorticoids
  • Ion transport
  • Mineralocorticoids
  • Na/K-ATPase

ASJC Scopus subject areas

  • Otorhinolaryngology

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