Beta-2 adrenergic receptors are $G_s$-coupled GPCRs. Their secondary messenger system operates through $\text{Adenylate Cyclase}$.
Signal transduction pathway:
$$\text{Beta-2 agonist} \rightarrow \text{Beta-2 receptor} \rightarrow G_s\text{-protein activation} \rightarrow \text{Adenylate Cyclase activation} \rightarrow \text{ATP} \rightarrow \text{cAMP} \rightarrow \text{PKA activation} \rightarrow \text{Cellular response}$$
Physiological effects mediated via cAMP (Beta-2):
- Bronchodilation (relaxation of bronchial smooth muscle)
- Uterine relaxation (tocolysis)
- Vasodilation in skeletal muscle
- Glycogenolysis in liver and muscle
Why not other options?
- Tyrosine kinase receptors: insulin, EGF, PDGF -- not adrenergic
- TGF-beta receptors: serine/threonine kinase, SMAD pathway
- Cytokine receptors: JAK-STAT signaling
Adrenergic receptor-G protein coupling summary:
- $\alpha_1$: $G_q$ (IP3/DAG pathway)
- $\alpha_2$: $G_i$ (inhibits adenylate cyclase)
- $\beta_1, \beta_2, \beta_3$: $G_s$ (stimulates adenylate cyclase -- cAMP)
\[\boxed{\text{Adenylate Cyclase (cAMP pathway)}}\]