In guinea-pig ventricular myocytes, Na+ influx via Na+ channels modulates Ca2+ release by affecting SR Ca2+ load rather than acting as a direct trigger during action potentials.
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Challenges assumed Na+ channel Ca2+ entry as SR trigger in ventricular myocytes; leaves open INa modulation of SR load in human cardiomyocytes.
Sipido et al. (1995) studied this question.
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