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JCI Table of Contents, 15 August 2003

rd School of Public Health and Brigham and Women's Hospital in Boston, Massachusetts, discuss additional explanations for the bronchoconstricting effects associated with chronic beta2AR stimulation. The commentary authors state that "it is interesting to note that the adverse effects of regular b-agonist use can be observed even weeks after their withdrawal, at a time when beta2AR desensitization should be resolved". These authors also indicate that studies of regular beta-agonist use have reported adverse effects only in subjects with a particular mutation in the beta2AR. The impact of this mutation has not been fully examined in any cell type.

Liggett and his research team suggest that therapeutics targeting PLCb may have substantial benefit in the treatment of asthma, particularly when chronic beta-agonist use is prescribed. Shore and Drazen suggest that it is possible that this is "just the tip of the iceberg" and that "understanding the panoply of beta2AR-mediated events in airway smooth muscle might lead to the design of new agonists that avoid negative effects of beta2AR activation while enhancing events that lead to relaxation".

TITLE: Antithetic regulation by beta-adrenergic receptors of Gq receptor signaling via phospholipase C underlies the airway beta-agonist paradox

AUTHOR CONTACT:
Stephen B. Liggett
University Of Cincinnati, Cincinnati, Ohio, USA.
Phone: (513) 558-4831
Fax 1: (513) 558-0835
E-mail: stephen.liggett@uc.edu

View the PDF of this article at: https://www.the-jci.org/press/18193.pdf

ACCOMPANYING COMMENTARY:
Beta-agonists and asthma: too much of a good thing?

AUTHOR CONTACT:
Stephanie Shore
Harvard School of Public Health, Boston, Massachusetts, USA.
Phone 1: (617) 432-0199
Fax 1: (617) 432-3468
E-mail:

Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Aug-2003


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