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Published ahead of print on February 5, 2003, doi:10.1164/rccm.200201-055OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 8, April 2003, 1102-1108

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Submitted on January 30, 2002
Accepted on February 4, 2003

Neurokinins Modulate Hyperventilation-Induced Bronchoconstriction in Canine Peripheral Airways

Arthur N Freed1*, Sharron McCulloch1, Teresa Meyers1, and Ryoichi Suzuki1

1 Environmental Health Sciences, Johns Hopkins University, School of Public Health, Baltimore, MD, USA

* To whom correspondence should be addressed. E-mail: freeda{at}nhlbi.nih.gov.

This study was designed to test the hypotheses that 1) neurokinin (NK) receptor activity modulates hyperventilation-induced bronchoconstriction (HIB) in canine peripheral airways, and 2) NK-receptor activity is stimulated via hyperventilation-induced eicosanoid production and release. A bronchoscope was used in anesthetized dogs to record peripheral airway resistance (Rp), test airway reactivity to neurokinin A (NKA), substance P (SP), and hypertonic saline (HS), and to examine HIB before and after combined treatment with NK-1 (CP 99994) and NK-2 (SR 48968) receptor antagonists. Bronchoalveolar lavage fluid (BALF) cells, prostaglandin D2, and cysteinyl-leukotrienes from hyperventilated airways pretreated with either vehicle or NK antagonists were also measured. Pretreatment with NK-1 and NK-2 antagonists significantly attenuated HIB and the response to SP, virtually abolished the response to NKA, and had little effect on the response to HS. Blockade of NK-1 and NK-2 receptors did not affect either the cell profiles or the mediator concentrations recovered in BALF after hyperventilation. We conclude that neurokinins modulate the development of HIB and appear to do so via hyperventilation-induced eicosanoid production and release.
Key words: Animal model, Exercise-Induced Asthma, Neurokinins




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