Beta2 receptors interact with which G protein leading to increased cAMP levels?

Beta2 adrenergic receptors are coupled to the Gs protein, which plays a crucial role in signal transduction. When a ligand binds to the beta2 receptor, it activates the associated Gs protein. The activated Gs protein then stimulates adenylate cyclase, an enzyme responsible for converting ATP to cyclic AMP (cAMP).

The increase in cAMP levels leads to various physiological effects, such as smooth muscle relaxation, increased heart rate, and enhanced metabolic processes. This mechanism is pivotal in the action of various medications, particularly bronchodilators used in conditions like asthma and chronic obstructive pulmonary disease (COPD), which utilize the beta2 receptor pathway to induce relaxation of bronchial smooth muscle.

In contrast, the other G proteins mentioned, such as Gi, Gq, and G12, have different roles. Gi typically inhibits adenylate cyclase, leading to decreased levels of cAMP, while Gq activates phospholipase C resulting in increased inositol trisphosphate (IP3) and diacylglycerol (DAG) pathways, and G12 is associated with different cellular functions, often involving cytoskeletal rearrangements.