In compensated cardiac hypertrophy the amplitude of Ca²⁺ transients is maintained or even larger than in control conditions. This is also observed in the dog with chronic atrioventricular (cAVB) block for 6 weeks. We studied the feedback of Ca²⁺ release from the sarcoplasmic reticulum on Ca²⁺ current inactivation and recovery, in particular during low plateau potentials in isolated LV midmyocardial myocytes from cAVB dogs, compared to weight-matched controls (CTRL). In the presence of beta-adrenergic stimulation with isoproterenol, we observed large window Ca²⁺ currents. These window currents were of equal magnitude in both groups, but the maximal current occurred at more positive potentials in cAVB. Window currents were accompanied by significant Ca²⁺ influx. Using a specific double clamp voltage protocol, we could quantify the availability of Ca²⁺ channels during and following Ca²⁺ release from the sarcoplasmic reticulum at steady membrane potential. Ca²⁺ release from the sarcoplasmic reticulum induced a pronounced degree of inactivation of the Ca²⁺ current followed by a significant recovery. This dynamic modulation was more pronounced in cAVB and could contribute to the higher incidence of early afterdepolarizations in cAVB. This is further discussed as part of the arrhythmic mechanisms in cardiac hypertrophy and contrasted to what is seen in heart failure.