Abstract
Background: The involvement of the airway smooth muscle mediator nitric oxide (NO) in the actions of the β<sub>2</sub> agonist salbutamol (Sal), a well- known bronchodilator, is very poorly understood. Objectives: To determine if endogenous NO release is a major factor in the Sal-induced relaxation of the carbachol- and electrical field-stimulated rat trachea and determine the role of the tracheal epithelium as the possible source of NO involved in these effects. Methods: Isolated carbachol- or electric field-stimulated pre-contracted in vitro male Sprague Dawley rat tracheas (with epithelium intact or denuded) were relaxed with incremental or discrete concentrations of Sal in the presence and absence of the NO synthesis inhibitor L-NAME. Results: Epithelium-denuded tracheas showed a reduced relaxation response to Sal. L-NAME (1 mM) similarly decreased the sensitivity of the rat tracheas to Sal in both epithelium-intact and -denuded conditions. In the presence of L-NAME, high concentrations of Sal induced an unexpectedly large relaxation response in carbachol-stimulated rat tracheas with both intact and denuded epithelium. Sal relaxation was also affected by L-NAME in electrical field-stimulated epithelium-intact and -denuded tracheas. Conclusion: The results suggest that NO derived from sources other than the epithelium is an important mediator of the Sal-induced relaxation in rat tracheas.
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