Background and purpose: β ₁- and β ₂- adrenoceptors coexist in rat heart but β ₂-adrenoceptor-mediated inotropic effects are hardly detectable, possibly due to phosphodiesterase (PDE) activity. We investigated the influence of the PDE3 inhibitor cilostamide (300 nmol·L ^-1) and the PDE4 inhibitor rolipram (1 ̄mol·L ^-1) on the effects of (-)-catecholamines. Experimental approach: Cardiostimulation evoked by (-)-noradrenaline (ICI118551 present) and (-)-adrenaline (CGP20712A present) through β ₁- and β ₂-adrenoceptors, respectively, was compared on sinoatrial beating rate, left atrial and ventricular contractile force in i/ated tissues from Wistar rats. L-type Ca ²⁺-current (I _Ca-L) was assessed with whole-cell patch clamp. Key results: Rolipram caused sinoatrial tachycardia. Cilostamide and rolipram did not enhance chronotropic potencies of (-)-noradrenaline and (-)-adrenaline. Rolipram but not cilostamide potentiated atrial and ventricular inotropic effects of (-)-noradrenaline. Cilostamide potentiated the ventricular effects of (-)-adrenaline but not of (-)-noradrenaline. Concurrent cilostamide + rolipram uncovered left atrial effects of (-)-adrenaline. Both rolipram and cilostamide augmented the (-)-noradrenaline (1 ̄mol·L ^-1) evoked increase in I _Ca-L. (-)-Adrenaline (10 ̄mol·L ^-1) increased I _Ca-L only in the presence of cilostamide but not rolipram. Conclusions and implications: PDE4 blunts the β ₁-adrenoceptor- mediated inotropic effects. PDE4 reduces basal sinoatrial rate in a compartment distinct from compartments controlled by β ₁- and β ₂-adrenoceptors. PDE3 and PDE4 jointly prevent left atrial β ₂-adrenoceptor-mediated inotropy. Both PDE3 and PDE4 reduce I _Ca-L responses through β ₁-adrenoceptors but the PDE3 component is unrelated to inotropy. PDE3 blunts both ventricular inotropic and I _Ca-L responses through β ₂-adrenoceptors.