Which agonist would most likely cause bronchial dilation?

Bronchial dilation is primarily mediated by the activation of beta-2 adrenergic receptors. When beta-2 agonists bind to these receptors, which are predominantly found in the smooth muscle lining the airways, they initiate a signal transduction pathway that promotes relaxation of the smooth muscle. This relaxation results in the widening of the bronchial passages, which improves airflow and is particularly beneficial in conditions such as asthma or chronic obstructive pulmonary disease (COPD).

In contrast, the other types of adrenergic receptors mentioned do not primarily facilitate bronchial dilation. Alpha-1 receptors, when activated, typically lead to vasoconstriction and can potentially narrow the airways. Alpha-2 receptors primarily play a role in inhibiting neurotransmitter release and do not contribute significantly to bronchodilation. Beta-1 receptors mainly influence cardiac function, increasing heart rate and contractility, and are not involved in the relaxation of bronchial smooth muscle. Therefore, the action of beta-2 agonists is specifically suited for inducing bronchial dilation.