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Articles in PresS, published online ahead of print December 7, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00319.2001
Submitted on August 10, 2001
Accepted on November 25, 2001
1 Internal Medicine and Radiology, University of Iowa College of Medicne, Iowa City, IA, USA; Research Service, Veterans Affairs Medical Center, Iowa City, IA, USA
2 Internal Medicine and Radiology, University of Iowa College of Medicne, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: stephen-mcgowan{at}uiowa.edu.
Vitamin A deficiency (VAD) remains an important health problem among children in developing countries. Children living in these areas have a higher mortality from respiratory infections, which likely results in part from suboptimal nutrition, including VAD. Bronchial hyperreactivity can follow viral respiratory infections and may complicate the recovery. To investigate whether VAD promotes bronchial hyperreactivity we have assessed bronchoconstriction that is induced by methacholine in vitamin A deficient and vitamin A sufficient (VAS) rats. VAD rats developed bronchial constriction at lower concentrations of inhaled methacholine than VAS rats did. This did not result from an increase in the bronchial wall thickness or the clearance of a small molecule (with a size similar to methacholine) from the airspace. The function and abundance of the muscarinic-2 receptors in bronchial tissue were reduced in VAD rats, suggesting that this receptor may contribute to these animals' diminished ability to limit cholinergic-mediated bronchoconstriction. A similar reduction in muscarinic-2 receptor function has been observed in asthma. Vitamin A (retinol) and its congeners (retinoids) may be required to regulate bronchial responsiveness in addition to maintaining a normal bronchial epithelium.
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