All use cAMP as second messenger during their physiological functions, EXCEPT:

Activation of D1-type receptors leads to an increase in cAMP, whereas activation of D2-like receptors reduces cAMP levels. ACTH binds to high-affinity plasma membrane receptors, thereby activating adenylyl cyclase and increasing cyclic adenosine monophosphate, which in turn activates intracellular phosphoprotein kinases. In the liver, glucagon acts Gs to activate adenylyl cyclase and increase intracellular cAMP. This leads protein kinase A to activation of phosphorylase. The V2 receptors of vasopressin act through Gs to increase cyclic adenosine 3',5'-monophosphate (cAMP) levels. Ref: Barrett K.E., Barman S.M., Boitano S., Brooks H.L. (2012). Chapter 7. Neurotransmitters & Neuromodulators. In K.E. Barrett, S.M. Barman, S. Boitano, H.L. Brooks (Eds), Ganong's Review of Medical Physiology, 24e.