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The effect of temperature on the rate-dependent decrease of the rat ventricular calcium current

S O McMorn1, S M Harrison, M R Boyett

  • 1Department of Physiology, University of Leeds, UK.

Experimental Physiology
|March 4, 1998
PubMed
Summary
This summary is machine-generated.

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Temperature significantly impacts the rate-dependent decrease in L-type Ca2+ current (iCa) in rat heart cells. Lower temperatures exacerbate iCa decline due to slower channel recovery from inactivation.

Area of Science:

  • Cardiovascular Physiology
  • Ion Channel Biophysics
  • Cellular Electrophysiology

Background:

  • L-type Ca2+ current (iCa) is crucial for cardiac excitation-contraction coupling.
  • Rate-dependent changes in iCa can affect heart function under physiological and pathological conditions.
  • Temperature is a known modulator of ion channel kinetics.

Purpose of the Study:

  • To investigate the influence of temperature on the rate-dependent reduction of L-type Ca2+ current (iCa) in rat ventricular myocytes.
  • To elucidate the underlying mechanisms of temperature-dependent iCa decline during rapid stimulation.

Main Methods:

  • Isolated rat ventricular myocytes were used to measure L-type Ca2+ current (iCa).
  • Electrophysiological techniques, including whole-cell patch-clamp and cell-attached patches, were employed.

Related Experiment Videos

  • Experiments were conducted at different temperatures (22°C and 37°C) with varying stimulation rates (0.5 Hz to 3.0 Hz).

    • Main Results:

    • Increasing stimulation rate from 0.5 to 3.0 Hz induced a reversible decrease in iCa, which was temperature-dependent.
    • At 22°C, the initial decrease in iCa at 3 Hz was significantly larger (38%) compared to 37°C (9%).
    • Slower recovery from fast inactivation at 22°C, compared to 37°C, explained the greater initial iCa decline, with a Q10 of 5.6 for recovery.

    Conclusions:

    • Temperature significantly modulates the rate-dependent decrease in L-type Ca2+ current (iCa) in ventricular myocytes.
    • The primary mechanism for the enhanced iCa decline at lower temperatures is slowed recovery from fast inactivation.
    • The progressive, secondary decrease in iCa shows less temperature dependence, suggesting different inactivation mechanisms are involved.