What intracellular messenger is known to promote bronchodilation?

The intracellular messenger that promotes bronchodilation is increased cAMP (cyclic adenosine monophosphate). cAMP plays a critical role in the relaxation of bronchial smooth muscle, leading to dilation of the airways. When cAMP levels rise within cells, it activates protein kinases that lead to the phosphorylation of specific proteins involved in muscle relaxation. This mechanism is particularly important in the action of bronchodilator medications, such as beta-agonists, which stimulate adrenergic receptors. The activation of these receptors increases cAMP levels, directly facilitating bronchodilation.

In contrast, other options do not primarily promote bronchodilation. For instance, cyclic GMP is generally associated with vasodilation and other cellular processes that do not directly lead to bronchodilation. Calcium ions, on the other hand, when increased intracellularly, typically lead to muscle contraction, which would have the opposite effect of promoting bronchoconstriction rather than bronchodilation. Lastly, while changes in potassium levels are involved in various cellular functions, they do not have a direct and primary role in promoting bronchodilation as cAMP does. Thus, increased cAMP is the key messenger that specifically promotes this desired effect in the respiratory system.