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Is a myogenic response involved in deep inspiration-induced bronchoconstriction in asthmatics?
1Laboratoire de Physiologie, Université de Bordeaux II, France.
Abstract:
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.
Insights
Nifedipine, a calcium channel blocker, reduced deep inspiration-induced bronchoconstriction in asthmatic patients. This suggests a myogenic response in asthma, potentially linked to airway smooth muscle changes.
Area of Science:
- Respiratory Medicine
- Pharmacology
- Physiology
Background:
- Deep inspiration (DI) can trigger bronchoconstriction in some asthma patients, but the underlying mechanisms are not fully understood.
- A calcium-dependent myogenic response is a potential contributor to this phenomenon.
Purpose of the Study:
- To investigate the role of calcium channels in deep inspiration-induced bronchoconstriction in asthma.
- To examine the effect of nifedipine, a voltage-dependent calcium channel antagonist, on this response.
Main Methods:
- A placebo-controlled study involving six asthmatic patients and six healthy controls.
- Nifedipine (20 mg sublingually) or placebo was administered before and after methacholine (MCh) challenge.
- Plethysmographic specific airway conductance (SGaw) was measured to assess airway response to DI.
Main Results:
- Nifedipine significantly reduced the decrease in SGaw induced by DI in asthmatic patients at baseline.
- Nifedipine did not affect baseline SGaw values or the DI-induced changes after MCh challenge in asthmatics.
- Nifedipine had no significant effect on DI-induced SGaw changes in healthy controls, before or after MCh.
Conclusions:
- Nifedipine mitigates deep inspiration-induced bronchoconstriction in asthma patients without altering baseline airway tone.
- This suggests a myogenic response in asthmatic airways, possibly due to a shift in airway smooth muscle function.
- The findings highlight a potential therapeutic target for managing DI-induced bronchoconstriction in asthma.