What evidence implicates airway smooth muscle in the cause of BHR?

Nickolai O. Dulin, Darren J. Fernandes, Maria Dowell, Shashi Bellam, John McConville, Oren Lakser, Richard Mitchell, Blanca Camoretti-Mercado, Paul Kogut, Julian Solway*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

39 Scopus citations


Bronchial hyperresponsiveness (BHR), the occurrence of excessive bronchoconstriction in response to relatively small constrictor stimuli, is a cardinal feature of asthma. Here, we consider the role that airway smooth muscle might play in the generation of BHR. The weight of evidence suggests that smooth muscle isolated from asthmatic tissues exhibits normal sensitivity to constrictor agonists when studied during isometric contraction, but the increased muscle mass within asthmatic airways might generate more total force than the lesser amount of muscle found in normal bronchi. Another salient difference between asthmatic and normal individuals lies in the effect of deep inhalation (DI) on bronchoconstriction. DI often substantially reverses induced bronchoconstriction in normals, while it often has much less effect on spontaneous or induced bronchoconstriction in asthmatics. It has been proposed that abnormal dynamic aspects of airway smooth muscle contraction - velocity of contraction or plasticity-elasticity balance - might underlie the abnormal DI response in asthma. We suggest a speculative model in which abnormally long actin filaments might account for abnormally increased elasticity of contracted airway smooth muscle.

Original languageEnglish (US)
Pages (from-to)73-84
Number of pages12
JournalClinical Reviews in Allergy and Immunology
Issue number1
StatePublished - Feb 2003


  • Actin
  • Asthma
  • Deep breath
  • Hyperresponsive
  • Inhalation

ASJC Scopus subject areas

  • Immunology and Allergy

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