help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Published ahead of print on July 10, 2008
Am. J. Respir. Cell Mol. Biol. 2008, doi:10.1165/rcmb.2008-0150OC
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Bosse, Y.
Right arrow Articles by Seow, C. Y
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bosse, Y.
Right arrow Articles by Seow, C. Y

Submitted on April 17, 2008
Revised on July 10, 2008

Adaptation of Airway Smooth Muscle to Basal Tone: Relevance to Airway Hyperresponsiveness

Ynuk Bosse1*, Leslie YM Chin2, Peter D Pare3, and Chun Y Seow2

1 University of British Columbia, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Providence Health Care/St.Paul's Hospital, Vancouver, British Columbia, Canada, 2 University of British Columbia, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Providence Health Care/St.Paul's Hospital, Vancouver, British Columbia, Canada; Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, 3 University of British Columbia, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Providence Health Care/St.Paul's Hospital, Vancouver, British Columbia, Canada; Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, British Columbia, Canada

* To whom correspondence should be addressed. E-mail: ybosse{at}mrl.ubc.ca.

Lung inflammation and airway hyperresponsiveness (AHR) are hallmarks of asthma but their interrelationship is unclear. Excessive shortening of airway smooth muscle (ASM) in response to bronchoconstrictors is likely an important determinant of AHR. Hyper- contractility of ASM could stem from a change in the intrinsic properties of the muscle, or it could be due to extrinsic factors such as chronic exposure of the muscle to inflammatory mediators in the airways. The latter could be the link between lung inflammation and AHR. The present study was designed to examine the influence of chronic exposure to a contractile agonist on the force-generating capacity of ASM. Force generation in response to electric field stimulation (EFS) was measured in ovine trachealis with or without a basal tone induced by acetylcholine (ACh). While the tone was maintained, the EFS-induced force decreased transiently but increased over time to reach a plateau in ~50 min. The total force (ACh tone + EFS force) increased monotonically and in proportion to ACh concentration. The results indicate that the muscle adapted to the basal tone and regained its contractile ability in response to a second stimulus (EFS) over time. Analysis suggests that this is due to a cytoskeletal transformation that allows the cytoskeleton to bear force thus freeing up actomyosin crossbridges to generate more force. Force adaptation in ASM as a consequence of prolonged exposure to the many spasmogens found in asthmatic airways could be a mechanism contributing to AHR seen in asthma.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2008 American Thoracic Society. 		  ATS Best of the Web