Figure 2.

Adrenergic receptor signaling and cross-talk with the renin-angiotensin aldosterone system. Activation of β-adrenergic receptor signaling increases cAMP levels and activates protein kinase A (PKA) to promote vasodilation and an increase in cardiac contractility. These effects are opposed by α₂-AR signaling. PKA also activates the MAP kinase signaling pathway, which is downstream from the angiotensin type 1 receptor (AT1R). AT1R also activates protein tyrosine kinases (PTK), which have been implicated in pulmonary hypertension, and similar to α₁-AR, activates phospholipase C (PLC). Both AT1R and mineralocorticoid receptor (MR) activate NADPH oxidase to increase reactive oxygen species formation (ROS), which decrease bioavailable nitric oxide (NO•).