Friction in airway smooth muscle: mechanism, latch, and implications in asthma.

Though its role in airway smooth muscle is not well established, recent research indicates that dystrophin along with other subunits of dystrophin glycoprotein complex is associated with phenotype maturation.

However, airway smooth muscle has demonstrated almost no capacity for regeneration, instead being replaced by connective tissue.

Leukotrienes cause tightening of airway muscles and the production of excess mucus and fluid.

Another problem for smokers: as nicotine levels drop during sleep, the airway muscles start to go slack.

For example in airway smooth muscles of humans and other species, generic PDE1 accounts for more than 50% of the hydrolytic activity of cyclic nucleotides.

It is taken in an inhaler and helps relax airway muscles.

Anticholinergic drugs cause airway smooth muscles to relax by blocking stimulation from cholinergic nerves.

It is caused by some problem in the central nervous system, most likely a failure of the brain to signal the airway muscles to breathe.

This is accomplished by the rhythmic contraction of upper airway muscles, such as the genioglossus (tongue) and the hyoid muscles.