Ipratropium exhibits broncholytic action by reducing cholinergic influence on the bronchial musculature. It blocks muscarinic acetylcholine receptors, without specificity for subtypes, and therefore promotes the degradation of cyclic guanosine monophosphate (cGMP), resulting in a decreased intracellular concentration of cGMP.  Most likely due to actions of cGMP on intracellular calcium, this results in decreased contractility of smooth muscle in the lung, inhibiting bronchoconstriction and mucus secretion . It is a nonselective muscarinic antagonist ,  and does not diffuse into the blood, which prevents systemic side effects. Ipratropium is a derivative of atropine  but is a quaternary amine and therefore does not cross the blood–brain barrier , which prevents central side effects (anticholinergic syndrome). Ipratropium is not considered a short-acting bronchodilator and should never be used in place of salbutamol (albuterol) as a rescue medication.
Whether airway hyperresponsiveness is a symptom of airway inflammation or airway remodeling, or whether it is the cause of long-term loss of lung function, remains controversial. Some investigators have hypothesized that aggressive treatment with anti-inflammatory therapies improves the long-term course of asthma beyond their salutary effects on parameters of asthma control and rates of exacerbation over time. 13 This contention has been supported by an observational study 14 that found long-term exposure to ICS was associated with an attenuation of the accelerated decline in lung function previously reported in asthmatics; more studies are required to substantiate these findings.