RAPGEF3 and atrial fibrillation: Next, we evaluated the role of PDEs in the control of basal cytosolic and local cAMP signaling (using the genetically encoded FRET-based sensors Epac1-camps, pm-Epac1 and Epac1-JNC) by inhibiting all PDEs expressed in the atria [22] using IBMX (100 μM) together with the PDE8 inhibitor PF-04957325 (100 nM), in atrial myocytes from Ctl and AF patients.