Growth hormone releasing hormone acts via G-coupled receptors. G coupled receptors need GTP to become activated and GTPase to become inactivated.

No GTP-ase --> chronically active growth hormone releasing hormone receptor --> constant activation of adenylyl cyclase / cAMP pathway and release of growth hormone.

The receptor in question is a G protein receptor on the pituitary mass. This would be the GHRH receptor. The GH receptor will be present downstream so that GH released from the pituitary can bind to it (these are JAK/STAT receptors). GHRH receptors are G¬s receptors. These receptors are bound at the alpha-subunit to GDP in the inactive state. When GHRH binds they activated when GTP attaches to the alpha-subunit instead. And thereby promotoes adenyl cyclase activity. GTPase is responsible to cleave this GTP from the alpha subunit to switch of the receptoe. Therefor a lack of GTPase activity will render he Gs receptor in a prolonged on state  Increased activity of Adenyl Cyclase.

Why is the answer adenylyl cyclase? I looked in FA and I saw that GH uses the JAK2/STAT pathway and that IGF-1 uses the MAP Kinase pathway. Not sure how adenylyl cyclase plays into this.