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Published on: May 19, 2017
Sarcoplasmic reticulum K(+) (TRIC) channel does not carry essential countercurrent during Ca(2+) release
Tao Guo1, Alma Nani, Stephen Shonts
1Department of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, Illinois, USA.
Biophysical Journal
|September 10, 2013
Summary
The sarcoplasmic reticulum K(+) (TRIC) channel is not essential for calcium release or uptake. Instead, it likely restores potassium balance after calcium release channels close, maintaining sarcoplasmic reticulum membrane potential.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
- Ion Channel Function
Background:
- Sarcoplasmic reticulum (SR) Ca(2+) efflux requires compensatory SR K(+) influx to maintain membrane potential (Vm) and allow sustained Ca(2+) release.
- The trimeric intracellular cation (TRIC) channel has been proposed to mediate this essential K(+) influx, but ryanodine receptors (RyRs) also conduct K(+) during Ca(2+) release.
Purpose of the Study:
- To investigate the physiological role of the SR K(+) (TRIC) channel in supporting SR Ca(2+) transport.
- To determine if TRIC channels are essential for maintaining SR Vm during Ca(2+) release.
Main Methods:
- Used saponin-permeabilized cardiomyocytes to study SR Ca(2+) transport.
- Manipulated SR K(+) channel function by altering cytosolic ion composition (K+ replaced with Na+ or Cs+).
- Measured Ca(2+) sparks, SR Ca(2+) reloading, and caffeine-evoked Ca(2+) release.
Main Results:
- Reducing SR K(+) channel conduction by 35% (with Na+) or 88% (with Cs+) did not affect Ca(2+) sparks, reloading, or release.
- Ryanodine receptor (RyR) function remained largely unaffected by the ionic manipulations.
- These findings indicate that TRIC-mediated K+ influx is not required for SR Ca(2+) release or uptake.
Conclusions:
- The SR K(+) (TRIC) channel is not essential for supporting SR Ca(2+) release or uptake.
- K+ influx through RyRs during Ca(2+) release compensates for Ca(2+) efflux.
- The TRIC channel's primary role is likely to restore trans-SR K+ balance after RyRs close, ensuring stable SR Vm near 0 mV.
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