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Alpha-adrenergic bronchoconstriction in man

R Marcelle1

  • 1Institut Léon Fredericq, Physiologie, Université de Liège, Belgium.

Archives of Physiology and Biochemistry
|December 1, 1996
PubMed
Summary
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Inhaled norepinephrine causes airway constriction in humans only after beta-blockers are administered. Asthmatics require lower beta-blocker doses, and alpha-blockers prevent this effect, revealing a balance of airway tone regulation.

Area of Science:

  • Pharmacology
  • Respiratory Physiology

Background:

  • The resting bronchial tone is influenced by adrenergic receptor activity.
  • Beta-adrenergic stimulation typically causes bronchodilation, while alpha-adrenergic stimulation can cause bronchoconstriction.

Purpose of the Study:

  • To investigate the role of alpha- and beta-adrenergic receptors in regulating airway tone in normal and asthmatic subjects.
  • To determine the effects of norepinephrine on airway resistance following beta-adrenergic blockade.

Main Methods:

  • Administration of inhaled norepinephrine (NE) to normal, asymptomatic, and asthmatic subjects.
  • Pretreatment with propranolol (a beta-receptor blocker) and phentolamine (an alpha-receptor blocker).
  • Measurement of airway resistance and respiratory asynchronism.

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Main Results:

  • In normal and asymptomatic subjects, inhaled NE induced bronchoconstriction and respiratory asynchronism only after propranolol pretreatment.
  • Asthmatic subjects required lower doses of propranolol to reveal NE-induced constrictive properties.
  • Phentolamine prevented the increases in airway resistance caused by NE after beta-blockade.

Conclusions:

  • The resting bronchial tone is tonically relaxed by beta-adrenergic receptor stimulation.
  • Suppression of beta-adrenergic activity unmasks an alpha-adrenergic-induced bronchoconstriction.
  • Bronchial relaxing properties mediated by beta-receptors predominate over constrictive properties mediated by alpha-receptors in normal airways.