Abstract
The origin of Ca 2+ contributing to the enhancement of acetylcholine-induced bronchial smooth muscle constriction in airway hyperresponsiveness induced by antigen challenge was investigated. Under Ca 2+-free (concomitant with 10 −6 M nicardipine) conditions, the contractile responses of bronchial rings to 1 mM acetylcholine were significantly greater in rings from rats with hyperresponsive airways (0.15 ± 0.04 g) than those of rings from normal rats (0.02 ± 0.004 g; P < 0.05). The cumulatively administered Ca 2+ induced a markedly greater bronchoconstriction in rings from rats with hyperresponsive airways in Ca 2+-free solution when muscles were pretreated with 1 mM acetylcholine (in the presence of 10 −6 M nicardipine) than in rings from normal rats, whereas no significant difference in Ca 2+-induced bronchoconstriction was observed between the two groups when muscles were pretreated with 60 mM K + (in the presence of 10 −6 M atropine). These findings suggest that enhancement of the availability of Ca 2+ released from intracellular stores and/or influxed through receptor-operated Ca 2+ channels in airway smooth muscles might be involved in the airway hyperresponsiveness to acetylcholine in rats.
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