Activation of the beta-2 adrenergic receptor on bronchial smooth muscle leads to bronchodilation through which intracellular messenger?

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Multiple Choice

Activation of the beta-2 adrenergic receptor on bronchial smooth muscle leads to bronchodilation through which intracellular messenger?

Explanation:
When beta-2 receptors on bronchial smooth muscle are activated, they couple to Gs proteins that stimulate adenylyl cyclase, increasing intracellular cyclic AMP. Elevated cAMP activates protein kinase A, which lowers the calcium level inside the cell and reduces the contractile machinery’s sensitivity to calcium. The net effect is relaxation of the airway smooth muscle, i.e., bronchodilation. This is the mechanism behind beta-2 agonists used in asthma and COPD. The other messengers describe pathways that typically promote contraction rather than dilation: IP3 releases calcium from intracellular stores, DAG activates PKC, and calcium itself is a key driver of smooth muscle contraction.

When beta-2 receptors on bronchial smooth muscle are activated, they couple to Gs proteins that stimulate adenylyl cyclase, increasing intracellular cyclic AMP. Elevated cAMP activates protein kinase A, which lowers the calcium level inside the cell and reduces the contractile machinery’s sensitivity to calcium. The net effect is relaxation of the airway smooth muscle, i.e., bronchodilation. This is the mechanism behind beta-2 agonists used in asthma and COPD.

The other messengers describe pathways that typically promote contraction rather than dilation: IP3 releases calcium from intracellular stores, DAG activates PKC, and calcium itself is a key driver of smooth muscle contraction.

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