Role for Sodium Channels and Intracellular Sodium in Regulation of the Cardiac Force-Frequency Relation and Contractility

January, Craig T.; Fozzard, Harry A.

doi:10.1007/978-1-4613-1513-1_1

Cited by 1 publication

(1 citation statement)

References 25 publications

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“…Purkinje cells retain stable large-amplitude contractions when stimulated from rest or at low frequencies (see January and Fozzard, 1990), which is different from ventricular cells. Therefore, voltage clamp steps were applied at 0.1 Hz.…”

Section: Cell Shorteningmentioning

confidence: 99%

Both T- and L-Type Ca2+ Channels Can Contribute to Excitation-Contraction Coupling in Cardiac Purkinje Cells

Zhou

January

1998

Biophysical Journal

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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 depended 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.

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Section: Cell Shorteningmentioning

confidence: 99%