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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
Summary
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.
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.