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  • Title: Paradoxal effect of salbutamol in an in vitro model of bronchoprotection.
    Author: Girodet PO, Berger P, Martinez B, Marthan R, Advenier C, Molimard M.
    Journal: Fundam Clin Pharmacol; 2005 Apr; 19(2):179-86. PubMed ID: 15810898.
    Abstract:
    Salbutamol-induced hyperresponsiveness to acetylcholine was investigated in human and guinea-pig isolated airways and cultured human airway smooth muscle cells. Salbutamol (10(-7)-10(-5) m) inhibited contractions induced by low concentrations of acetylcholine (10(-8)-10(-7) m) but potentiated contractions induced by higher concentrations of acetylcholine (10(-5)-10(-3) m). Pretreatment with the calcium channel antagonist nicardipine suppressed salbutamol-induced hyperresponse. Stimulation of cultured human airway smooth muscle cells with salbutamol (10(-6) m) amplified intracellular calcium concentration rise induced by acetylcholine (10(-5) m). Propranolol (10(-7) m), a beta1- and beta2-adrenoceptor antagonist, and ICI 118551 (10(-7)-10(-6) m), a beta2-adrenoceptor antagonist, suppressed the inhibitory effect of salbutamol but did not inhibit the hyperresponse on high concentrations of acetylcholine. In contrast, higher concentration of propranolol (10(-6) m) inhibited salbutamol-induced hyperreactivity. Effects of salbutamol were not affected by atenolol, a beta1-adrenoceptor blocker. Salbutamol-induced hyperresponsiveness is mediated through a mechanism involving calcium channel activation.
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