Beta 2-adrenoceptor agonist-mediated inhibition of human airway smooth muscle cell proliferation: importance of the duration of beta 2-adrenoceptor stimulation

British Journal of Pharmacology
A G StewartJ Wilson

Abstract

1. Airway hyperresponsiveness in asthma has been ascribed to airway wall thickening as a result of smooth muscle proliferation and hypertrophy. We have previously shown that continuous exposure to the beta 2-adrenoceptor agonist, salbutamol inhibits mitogen-induced proliferation of airway smooth muscle cells. In the present study, the effects of variable durations and repeated periods of exposure to beta 2-adrenoceptor agonists on DNA synthesis in human cultured airway smooth muscle have been investigated to model some of the possible pharmacokinetic profiles of these agents following inhalation. DNA synthesis was measured by [3H]-thymidine incorporation. 2. Shorter periods of exposure (up to 2.5 h) of airway smooth muscle cells to salbutamol (100 nM) commencing 30 min before thrombin (0.3 u ml-1) stimulation had no effect on the subsequent increase in [3H]-thymidine incorporation. However, inhibition by salbutamol was evident with a 4.5 h exposure and was maximal after an 8.5 h exposure. Similar patterns of results were observed when fenoterol (100 nM) was used in place of salbutamol as the beta 2-adrenoceptor agonist or when epidermal growth factor (300 pM) was used in place of thrombin as the mitogen. Salbutamol had no effec...Continue Reading

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