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Nonadrenergic, noncholinergic airway inhibitory nerves
J W Lammers1, P J Barnes, K F Chung
1Dept of Pulmonary Diseases Academic Hospital, University of Nijmegen, The Netherlands.
The European Respiratory Journal
|February 1, 1992
Summary
Nonadrenergic, noncholinergic (NANC) nerves in the airways cause muscle relaxation. While their role in mild asthma is similar to normal subjects, severe asthma shows reduced neuropeptide levels, suggesting altered function.
Area of Science:
- Respiratory physiology
- Neuropharmacology
- Pulmonary medicine
Background:
- Nonadrenergic, noncholinergic (NANC) nerves are known to relax airway smooth muscle across species.
- Vagal nerve stimulation and irritant challenges induce bronchodilation in cats and humans, even with blocked adrenergic and cholinergic pathways.
Purpose of the Study:
- To investigate the role and neurotransmitters of NANC inhibitory nerves in airway smooth muscle.
- To explore the function of NANC nerves in physiological and pathophysiological conditions like asthma.
Main Methods:
- Stimulation of efferent vagus nerves during cholinergic and adrenergic blockade.
- Capsaicin inhalation and mechanical laryngeal irritation under blockade conditions.
- Measurement of bronchodilator responses and neuropeptide (VIP, PHM) levels.
Main Results:
- NANC nerve stimulation causes significant bronchodilation in cats and transient bronchodilation in humans.
- Neuropeptides like VIP and PHM, and nitric oxide are potential NANC neurotransmitters, though not definitively proven.
- NANC bronchodilator response is comparable in mild asthma and normal subjects, but VIP immunoreactivity is reduced in severe asthma.
Conclusions:
- NANC inhibitory nerves play a role in airway smooth muscle relaxation.
- The function of NANC nerves may be altered in severe asthma, potentially involving reduced neuropeptide levels.
- Further research using molecular techniques and antagonists is needed to fully define the physiological and pathophysiological roles of these nerves.