Abstract
Recent evidence gathered in ventricular myocytes from rodents points out that the EPAC pathway is a strong promoter of the release of Ca2+ from the sarcoplasmic reticulum (SR; Pereira et al., 2007, J. Physiol. 583:685-94). Encouraged by the above observations, we studied the effects of 2 μM 8-CPT (a specific EPAC activator) on the diastolic SR Ca2+ release in rabbit ventricular myocytes. Our initial studies used epifluorescence and focused on the relationship between the SR load and the diastolic SR Ca2+ release (i.e., the so called SR Ca2+ leak-load relationship). Contrary to the observations in rodents, our rabbit ventricular myocytes displayed no alterations of the leak-load relationship upon 8-CPT application. Since the leak-load relationship requires a steady state to be reached prior to the measurements, we also tested for non steady-state effects of EPAC stimulation using confocal microscopy. We studied the frequency and properties of Ca2+ sparks during the first 30 seconds of rest decay following 2 minutes of 8-CPT application and field stimulation at 1 Hz. Our results showed no effects of EPAC stimulation on the spark frequency or the spatio-temporal properties of the sparks. In summary, our results suggest that EPAC does not affect diastolic SR Ca2+ release in rabbit ventricular myocytes. Future studies will target the species dependence of the effect of EPAC and the effect of SR [Ca2+] upon the release properties under these conditions.
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