Galindo-Tovar et al. (2009) argued that the lack of potentiation of the chronotropic effects of rolipram, cilostamide, and concurrent rolipram and cilostamide means that the cAMP pool governing H2-receptor-mediated sinoatrial tachycardia is protected from PDE3 and PDE4 and represents a compartment distinct from the cAMP compartment in which both PDE3 and PDE4 reduce basal sinoatrial beating. This evidence concerns the gene PDE4A and Tachycardia.