Key result
The skeletal muscle L-type channel is a major contributor to the Ca(2+) entry attributed to excitation-coupled Ca(2+) entry, as demonstrated by its inhibition by nonspecific cation channel antagonists.
Population
Skeletal muscle cells (normal myotubes and dysgenic myotubes expressing SkEIIIK)
Comparison
Pharmacological agents and external Ca2+ removal vs Untreated conditions or normal external Ca2+
Design
Preclinical
Authors
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Should not change clinical practice; leaves open L-type channel contribution to human excitation-coupled Ca(2+) entry.
The skeletal muscle L-type calcium channel is a major contributor to excitation-coupled calcium entry, clarifying the mechanisms of calcium influx during prolonged depolarization.
Bannister et al. (2008) studied this question. Pharmacological agents (2-APB, SKF 96356, La(3+), Gd(3+), dantrolene, nifedipine) was evaluated on L-type Ca(2+) current inhibition and Ca(2+) transient contribution. The skeletal muscle L-type channel is a major contributor to the Ca(2+) entry attributed to excitation-coupled Ca(2+) entry, as demonstrated by its inhibition by nonspecific cation channel antagonists.
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