Activated GPCRs cause a conformational change in the attached G protein complex, which results in the G alpha subunit's exchanging GDP for GTP and separation from the beta and gamma subunits. The G alpha subunit, in turn, activates adenylyl cyclase, which quickly converts ATP into cAMP. This leads to the activation of the cAMP-dependent pathway.  This pathway can also be activated downstream by directly activating adenylyl cyclase or PKA.
Molecules that activate cAMP pathway include:
* cholera toxin - increases cAMP levels
* forskolin - a diterpene natural product that activates adenylyl cyclase
* caffeine and theophylline inhibit cAMP phosphodiesterase, which degrades cAMP - thus enabling higher levels of cAMP than would otherwise be had. 
* bucladesine (dibutyryl cAMP, db cAMP) - also a phosphodiesterase inhibitor
* pertussis toxin, which increases cAMP levels by inhibiting Gi to its GDP (inactive) form. This leads to an increase in adenylyl cyclase activity, thereby increasing cAMP levels, which can lead to an increase in insulin and therefore hypoglycemia