What is the mechanism of action of inhaled anticholinergic bronchodilators such as ipratropium and tiotropium?

They block muscarinic receptors to reduce bronchoconstriction

Blocking muscarinic receptors in the airways prevents acetylcholine from triggering the vagal reflex that normally causes bronchoconstriction. These inhaled anticholinergic drugs act mainly on M3 receptors on airway smooth muscle; by occupying those sites, they stop acetylcholine from binding, so the smooth muscle relaxes and the airways dilate. They also reduce glandular secretions to some extent, which helps with airflow. Tiotropium stays bound longer and dissociates slowly, giving a long-acting effect, while ipratropium is shorter-acting. This mechanism is different from beta-adrenergic agonists, which stimulate beta receptors to cause relaxation, and from actions on nicotinic receptors at the neuromuscular junction, which these drugs do not affect. They also do not increase mucus production; if anything, they lessen cholinergic-driven secretions.

They stimulate beta-adrenergic receptors to increase heart rate

They inhibit nicotinic receptors in skeletal muscle

They increase mucus production

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