What is the mechanism of action by which inhaled anticholinergics produce bronchodilation?

Inhaled anticholinergics produce bronchodilation by blocking muscarinic receptors in the airways, which inhibits the action of acetylcholine and reduces smooth muscle contraction. Acetylcholine is a neurotransmitter that binds to muscarinic receptors on airway smooth muscle cells. When acetylcholine binds to these receptors, it triggers a cascade of events that lead to smooth muscle contraction, resulting in bronchoconstriction (narrowing of the airways). Anticholinergics, also known as muscarinic antagonists, competitively bind to these muscarinic receptors, preventing acetylcholine from binding. By blocking the action of acetylcholine, anticholinergics inhibit smooth muscle contraction and promote bronchodilation, widening the airways and reducing airway resistance. The primary muscarinic receptors involved in bronchoconstriction are M3 receptors, so anticholinergics that are selective for M3 receptors may be more effective in producing bronchodilation. Examples of inhaled anticholinergics include ipratropium bromide and tiotropium bromide. These medications are commonly used in the treatment of chronic obstructive pulmonary disease (COPD) to reduce bronchospasm and improve airflow.