Bronchial smooth muscle encircles the airways from the main bronchi to the terminal bronchioles, forming the dynamic diameter controller of the conducting airways. It has no role in gas exchange but determines the airway resistance that the respiratory muscles must overcome. Its hyperresponsiveness and hypercontractility defines asthma; its destruction by cigarette smoke and inflammation defines COPD.
| Location | Walls of the bronchi and bronchioles, as spiral bands between the lining and the cartilage, continuing to the respiratory bronchioles |
|---|---|
| Parts |
|
| Nerve Supply | Vagus nerve (parasympathetic, constricts); Sympathetic fibres (sparse; relaxation is mainly by circulating adrenaline on beta-2 receptors) |
| Blood Supply | Bronchial arteries |
Adjusts airway diameter and so airway resistance. Excess constriction narrows the airways in asthma, which is reversed by beta-2 agonist inhalers.
Asthma is characterised by bronchial smooth muscle hyperresponsiveness to triggers (allergens, cold air, exercise), producing acute bronchoconstriction reversible with beta-2 agonists. Short-acting beta-2 agonists (SABA, salbutamol) provide rapid bronchodilation; long-acting beta-2 agonists (LABA, salmeterol) provide sustained bronchodilation. Anticholinergics (ipratropium, tiotropium) block M3 muscarinic bronchoconstriction. In COPD, irreversible airflow limitation involves bronchial smooth muscle hypertrophy, fibrosis, and loss of elastic recoil. Bronchial thermoplasty uses radiofrequency energy to reduce bronchial smooth muscle mass in severe asthma.
Airway smooth muscle hyperresponsiveness to allergen triggers releases inflammatory mediators causing acute bronchoconstriction and mucosal oedema; forced expiratory volume in one second (FEV1) falls acutely and reverses with salbutamol inhaler; inhaled corticosteroids reduce smooth muscle inflammation and remodelling to prevent exacerbations.
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