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.
| Origin | Helical arrangement of smooth muscle fibres in the bronchial and bronchiolar walls, from the mainstem bronchi to the terminal bronchioles; the muscle wraps around the airway in a geodesic helical pattern |
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| Insertion | Continuous with the airway smooth muscle cells via gap junctions throughout the bronchial tree; no discrete tendinous insertion |
| Nerve Supply | Vagus nerve parasympathetic — bronchoconstriction via M3 muscarinic receptors; Sympathetic via beta-2 adrenergic receptors — bronchodilation; Non-adrenergic non-cholinergic (NANC) system — bronchodilation via VIP and NO |
| Blood Supply | Bronchial arteries (from descending aorta or intercostal arteries) |
| Actions | Bronchoconstriction narrows the airway lumen, increasing airway resistance and the work of breathing; bronchodilation widens the lumen, reducing resistance; smooth muscle tone is the primary determinant of airway calibre and is the main target of asthma therapy |
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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.
