A multitude of natural and pharmacological agents, including hormones, neurotransmitters, and phosphodiesterase inhibitors, raise intracellular cAMP levels and, in the vast majority of instances, the physiological effects are the result of activation of cAMP-dependent protein kinase (cA-PrK) and subsequent protein phosphorylation. The involvement of cA-PrK in the response may be investigated by the use of the “cA-PrK activity ratio” assay, first introduced in 1973 (1 ).
