Clinical meaning
Respiratory pharmacotherapy targets specific pathophysiological mechanisms of airway disease. Beta-2 agonists (albuterol, salmeterol, formoterol): activate beta-2 adrenergic receptors on airway smooth muscle → adenylyl cyclase activation → increased cAMP → smooth muscle relaxation (bronchodilation). Short-acting (SABA): onset 5-15 minutes, duration 4-6 hours (rescue use). Long-acting (LABA): onset 15-30 minutes (formoterol is faster), duration 12 hours (maintenance). Muscarinic antagonists (ipratropium, tiotropium): block M3 muscarinic acetylcholine receptors on bronchial smooth muscle, preventing vagally-mediated bronchoconstriction and reducing mucus secretion. SAMA (ipratropium) lasts 6-8 hours; LAMA (tiotropium) lasts 24 hours. Inhaled corticosteroids (ICS — fluticasone, budesonide, beclomethasone): suppress airway inflammation by inhibiting NF-kB-mediated transcription of pro-inflammatory cytokines, reducing eosinophilic infiltration, edema, and mucus hypersecretion. Leukotriene receptor antagonists (montelukast): block CysLT1 receptors, preventing leukotriene-mediated bronchoconstriction, inflammation, and mucus secretion; particularly effective in aspirin-exacerbated respiratory disease and exercise-induced asthma. Methylxanthines (theophylline): inhibit phosphodiesterase and block adenosine receptors, causing bronchodilation and mild anti-inflammatory effects; very narrow therapeutic index (10-20 mcg/mL) with significant drug interactions and toxicity (seizures, arrhythmias).