This study demonstrates that calcium influx through the calcium channel, rather than sodium current or sodium-calcium exchange, is the primary trigger for fast calcium release from the sarcoplasmic reticulum in cardiac myocytes.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications for myocyte calcium handling; leaves open translation of calcium-channel primacy to human physiology.
In cardiac myocytes, calcium influx through the calcium channel is the primary pathway for triggering calcium release. Recently it has been suggested that the calcium-induced calcium release mechanism can also be activated indirectly by the sodium current, which elevates the sodium concentration under the cell membrane, thereby favoring the entry of "trigger" calcium via the sodium-calcium exchanger. To test this hypothesis, sodium current was suppressed by reducing the external sodium concentration or applying tetrodotoxin. At potentials positive to -30 millivolts, calcium release was unaffected. A small calcium release at more negative potentials could be attributed to partial activation of calcium channels, because it was unaltered by replacement of sodium with lithium and was blocked by cadmium. Thus, sodium influx or its accumulation does not initiate calcium release. In addition, sodium-calcium exchange-related calcium release at potentials positive to +80 millivolts has slower kinetics than calcium channel-induced release. Therefore, only the calcium channel gates the fast release of calcium from the sarcoplasmic reticulum in the range of the action potential.
No takes yet. Share an insight, caveat, or question.
Sham et al. (1992) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: