Is a myogenic response involved in deep inspiration-induced bronchoconstriction in asthmatics?

The mechanisms by which a deep inspiration (DI) induces bronchoconstriction in some asthmatic patients remain unclear. As a calcium-dependent myogenic response could be involved, we examined the effect of a potent voltage-dependent calcium channel (VDC) antagonist, nifedipine (20 mg administered sublingually) versus placebo, on the DI-induced change in plethysmographic specific airway conductance (SGaw) in six asthmatic patients and six healthy controls both before and after a bronchial challenge with methacholine (MCh). In the asthmatic group, when compared to those receiving placebo, nifedipine significantly reduced the decrease in SGaw induced by the DI at baseline (-34.2 +/- 5.6 and -12.7 +/- 3.6%, respectively) but it had no significant effect on mean SGaw baseline values (0.096 +/- 0.018 and 0.075 +/- 0.015 cm H2O-1.s.-1, respectively). When airway tone was increased with MCh, the DI-induced change in SGaw was reduced and nifedipine then had no further effect. In the control group, nifedipine had no significant effect on the weak changes in SGaw induced by the DI before or after the bronchial challenge. We conclude that nifedipine reduces DI-induced bronchoconstriction only in subjects with asthma and without altering baseline tone in airway smooth muscle. We suggest that this effect of nifedipine could be explained by the existence of a myogenic response in asthma, caused by the conversion of airway smooth muscle from intermediate to single unit function.