A possible role of sarcoplasmic Ca2+ release in modulating the slow Ca2+ current of skeletal muscle

Ca2+ channels are regulated in a variety of different ways, one of which is modulation by the Ca2+ ion itself. In skeletal muscle, Ca2+ release sites are presumably located in the vicinity of the dihydropyridine-sensitive Ca2+ channel. In this study, we have tried to investigate the effects of Ca2+ release from the sarcoplasmic reticulum on the L-type Ca2+ channel in frog skeletal muscle, using the double Vaseline gap technique. We found an increase in Ca2+ current amplitude on application of caffeine, a well-known potentiator of Ca2+ release. Addition of the fast Ca2+ buffer BAPTA to the intracellular solution led to a gradual decline in Ca2+ current amplitude and eventually caused complete inhibition. Similar observations were made when the muscle fibre was perfused internally with the Ca2+ release channel blocker ruthenium red. The time course of Ca2+ current decline followed closely the increase in ruthenium red concentration. This suggests that Ca2+ release from the sarcoplasmic reticulum is involved in the regulation of L-type Ca2+ channels in frog skeletal muscle.