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Salbutamol is a beta(2)-adrenergic agonist and so it arouses beta(2)-adrenergic receptors. Binding of albuterol to beta(2)-receptors in the lungs results in relaxation of bronchial smooth muscles. It’s believed that salbutamol increases cAMP production by activating adenylate cyclase, and the activities of salbutamol are mediated by cAMP. Increased intracellular cyclic AMP increases the activity of cAMP-dependent protein kinase A, which inhibits the phosphorylation of myosin and reduces intracellular calcium levels. A lowered intracellular calcium concentration contributes to a smooth muscle relaxation and bronchodilation. Along with bronchodilation, salbutamol inhibits the discharge of bronchoconstricting agents from mast cells, inhibits microvascular leakage, and enhances mucociliary clearance.
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