Both T- and L-type Ca²⁺ channels can contribute to excitation- contraction coupling in cardiac Purkinje cells

Although L-type Ca²⁺ channels have been shown to play a central role in cardiac excitation-contraction (E-C) coupling, little is known about the role of T-type Ca²⁺ channels in this process. We used the amphotericin B perforated patch method to study the possible role of T-type Ca²⁺ current in E-C coupling in isolated canine Purkinje myocytes where both Ca²⁺ currents are large. T-type Ca²⁺ current was separated from L-type Ca²⁺ current using protocols employing the different voltage dependencies of the channel types and their different sensitivities to pharmacological blockade. We showed that Ca²⁺ admitted through either T- or L-type Ca²⁺ channels is capable of initiating contraction and that the contractions dependent on Ca²⁺-induced Ca²⁺ release from the sarcoplasmic reticulum (SR). The contractions, however, had different properties. Those initiated by Ca²⁺ entry through T-type Ca²⁺ channels had a longer delay to the onset of shortening, slower rates of shortening and relaxation, lower peak shortening, and longer time to peak shortening. These differences were present even when L-type Ca²⁺ current amplitude, or charge entry, was less than that of T- type Ca²⁺ current, suggesting that Ca²⁺ entry through the T-type Ca²⁺ channel is a less effective signal transduction mechanism to the SR than is Ca²⁺ entry through the L-type Ca²⁺ channel. We conclude that under our experimental conditions in cardiac Purkinje cells Ca²⁺ entry through the T- type Ca²⁺ channel can activate cell contraction. However, Ca²⁺ entry through the L-type Ca²⁺ channel is a more effective signal transduction mechanism. Our findings support the concept that different structural relationships exist between these channel types and the SR Ca²⁺ release mechanism.