Abstract
Prolonged use of β 2-adrenoceptor agonists has been associated with asthma exacerbation. Recently, phospholipase C-β1 (PLC-β1) induction in airway smooth muscle was proposed to underlie this phenomenon. We aimed to evaluate this mechanism in primary human airway smooth muscle cells. Stimulation of cells (1 μM isoprenaline or salbutamol for 2–48 h or 10 − 9 –10 − 4 M for 24 h) had no effect on PLC-β1 gene expression. 1 μM β 2-adrenoceptor agonist treatment for 24 h did not alter sodium fluoride Inositol Phosphate (IP) responses, however augmented histamine IP responses ( P < 0.05). Therefore, β 2-adrenoceptor agonists can augment spasmogen responses in airway smooth muscle but not via a G-protein/PLC-β1 mediated mechanism.
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