G activates the cAMP-dependent pathway by stimulating the production of cyclic AMP (cAMP) from ATP. This is accomplished by direct stimulation of the membrane-associated enzyme adenylate cyclase. cAMP can then act as a second messenger that goes on to interact with and activate protein kinase A (PKA). PKA can phosphorylate a myriad downstream targets.
The cAMP-dependent pathway is used as a signal transduction pathway for many hormones including:
* ADH – Promotes water retention by the kidneys (created by the magnocellular neurosecretory cells of the posterior pituitary)
* GHRH – Stimulates the synthesis and release of GH (somatotropic cells of the anterior pituitary)
* GHIH – Inhibits the synthesis and release of GH (somatotropic cells of anterior pituitary)
* CRH – Stimulates the synthesis and release of ACTH (anterior pituitary)
* ACTH – Stimulates the synthesis and release of cortisol (zona fasciculata of the adrenal cortex in the adrenal glands)
* TSH – Stimulates the synthesis and release of a majority of T4 (thyroid gland)
* LH – Stimulates follicular maturation and ovulation in women; or testosterone production and spermatogenesis in men
* FSH – Stimulates follicular development in women; or spermatogenesis in men
* PTH – Increases blood calcium levels.  This is accomplished via the parathyroid hormone 1 receptor (PTH1) in the kidneys and bones, or via the parathyroid hormone 2 receptor (PTH2) in the central nervous system and brain, as well as the bones and kidneys.
* Calcitonin – Decreases blood calcium levels (via the calcitonin receptor in the intestines, bones, kidneys, and brain)
* Glucagon – Stimulates glycogen breakdown in the liver
* hCG – Promotes cellular differentiation, and is potentially involved in apoptosis.
* Epinephrine – released by the adrenal medulla during the fasting state, when body is under metabolic duress.  It stimulates glycogenolysis, in addition to the actions of glucagon.