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Related Experiment Videos

Neurokinins modulate hyperventilation-induced bronchoconstriction in canine peripheral airways.

Arthur N Freed1, Sharron McCulloch, Teresa Meyers

  • 1Department of Environmental Heatlh Sciences, School of Public Health, The Johns Hopkins University, Baltimore, Maryland, USA. freeda@nhlbi.nih.gov

American Journal of Respiratory and Critical Care Medicine
|February 8, 2003
PubMed
Summary

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Neurokinins (NKs) modulate airway constriction during hyperventilation. Blocking NK-1 and NK-2 receptors reduced this response, suggesting a role in airway hyperreactivity.

Area of Science:

  • Respiratory Physiology
  • Pharmacology

Background:

  • Hyperventilation-induced bronchoconstriction (HIB) is a significant respiratory challenge.
  • Neurokinins (NKs) are implicated in airway inflammation and bronchoconstriction.

Purpose of the Study:

  • To investigate the role of neurokinin (NK) receptor activity in canine peripheral airway hyperresponsiveness during hyperventilation.
  • To determine if NK receptor activity is stimulated by hyperventilation-induced eicosanoid production.

Main Methods:

  • Anesthetized dogs underwent bronchoscopy to measure peripheral airway resistance (Rp).
  • Airway reactivity to NK A (NKA), substance P, and hypertonic saline was tested.
  • HIB was assessed before and after combined NK-1 and NK-2 receptor antagonist treatment.
  • Bronchoalveolar lavage fluid (BALF) cells, prostaglandin D2, and cysteinyl leukotrienes were measured.

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Main Results:

  • Combined NK-1 and NK-2 receptor antagonists significantly attenuated HIB and the response to substance P.
  • The response to NKA was nearly abolished, while the response to hypertonic saline was minimally affected.
  • NK receptor blockade did not alter BALF cell profiles or mediator concentrations post-hyperventilation.

Conclusions:

  • Neurokinins (NKs) play a modulatory role in the development of hyperventilation-induced bronchoconstriction (HIB).
  • NKs appear to mediate HIB through hyperventilation-induced eicosanoid production and release.