Alpha-adrenergic mRNA subtype expression in the human nasal turbinate.

Published

Journal Article

PURPOSE: Alpha-adrenergic receptor (AR) agonist drugs (e.g., epinephrine) are commonly used for upper airway procedures, to shrink the mucosa, retard absorption of local anesthetic agents, and improve visualization by limiting hemorrhage. Decongestant therapy often also includes alphaAR agonist agents, however overuse of these drugs (e.g., oxymetazoline) can result in chronic rhinitis and rebound increases in nasal secretion. Since current decongestants stimulate alphaARs non-selectively, characterization of alphaAR subtype distribution in human airway (nasal turbinate) offers an opportunity to refine therapeutic targets while minimizing side-effects. We, therefore, investigated alphaAR subtype expression in human nasal turbinate within epithelial, duct, gland, and vessel cells using in situ hybridization. METHODS: Since sensitive and specific anti-receptor antibodies and highly selective alphaAR subtype ligands are currently unavailable, in situ hybridization was performed on sections of three human nasal turbinate samples to identify distribution of alphaAR subtype mRNA. Subtype specific (35)S-labelled mRNA probes were incubated with nasal turbinate sections, and protected fragments remaining after RNase treatment analyzed by light and darkfield microscopy. RESULTS: In non-vascular tissue alpha(1d) AR mRNA predominates, whereas notably the alpha(2c) is the only alphaAR subtype present in the sinusoids and arteriovenous anastamoses. CONCLUSION: Combined with the current understanding that AR-mediated constriction of nasal sinusoids underpins decongestant therapies that minimize secretions and shrink tissues for airway procedures, these findings suggest that alpha(2c) AR subtypes provide a novel selective target for decongestant therapy in humans.

Full Text

Duke Authors

Cited Authors

  • Stafford-Smith, M; Bartz, R; Wilson, K; Baraniuk, JN; Schwinn, DA

Published Date

  • July 2007

Published In

Volume / Issue

  • 54 / 7

Start / End Page

  • 549 - 555

PubMed ID

  • 17602041

Pubmed Central ID

  • 17602041

International Standard Serial Number (ISSN)

  • 0832-610X

Digital Object Identifier (DOI)

  • 10.1007/BF03022319

Language

  • eng

Conference Location

  • United States