Pharmacology Notes

Beta₂-adrenergic agonists are minimally absorbed from the GI tract; inhaled forms exert their effects locally. After inhalation, beta₂-adrenergic agonists appear to be absorbed over several hours from the respiratory tract. These drugs don’t cross the blood-brain barrier; they’re extensively metabolized in the liver to inactive compounds and rapidly excreted in urine and stool.

Beta₂-adrenergic agonists increase levels of cyclic adenosine monophosphate by stimulating the beta₂-adrenergic receptors in the smooth muscle, resulting in bronchodilation. These drugs may lose their selectivity at higher doses, which can increase the risk of toxicity. Inhaled forms are preferred because they act locally in the lungs, resulting in fewer adverse reactions than systemically absorbed forms.

Short-acting inhaled beta₂-adrenergic agonists are the drugs of choice for fast relief of symptoms in the patient with asthma. They’re generally used as needed for asthma (including exercise-induced asthma) and COPD. A patient with COPD may use them around-the-clock on a specified schedule. However, excessive use of a short-acting beta₂-adrenergic agonist may indicate poor asthma control, requiring reassessment of the patient’s therapeutic regimen.

Long-acting beta₂-adrenergic agonists tend to be used with antiinflammatory agents, namely inhaled corticosteroids, to help control asthma.They’re especially useful for the patient with nocturnal asthmatic symptoms. These drugs must be administered on a schedule. They aren’t used to relieve acute symptoms because their onset of action isn’t fast enough. They also don’t affect the chronic inflammation associated with asthma.