Even though GC-A-stimulated cGMP microdomains seem to act differently than those stimulated by GC-B and do not seem to potentiate β-AR-stimulation of the cAMP pathway in several studies [53,62,98,106], some studies reported that GC-A stimulation can either reduce β-AR-mediated cAMP via PDE2 activation in nanodomains defined by a PKA RII-targeted biosensor [139] or increase the β-AR-mediated contractile effects in a mild hypertrophic model after TAC (transverse aortic constriction) [141]. This evidence concerns the gene ADRB2 and persistent truncus arteriosus.