Key result
Endothelin-1 exposure potentiated depolarization-induced Ca2+ influx in coronary smooth muscle cells by 31% and increased single cell phosphotyrosine by 95%.
Tyrosine phosphorylation of proteins other than voltage-gated calcium channels is necessary for prolonged potentiation by ET-1 of depolarization-induced Ca2+ influx in coronary smooth muscle.
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May implicate tyrosine phosphorylation in ET-1 coronary effects; leaves open translation to human vessels or clinical relevance.
Lee et al. (2002) studied this question. Endothelin-1 (ET-1) vs. Control was evaluated on Myoplasmic free Ca2+ ([Ca2+]m) responses to depolarization and tyrosine phosphorylation. Endothelin-1 exposure potentiated depolarization-induced Ca2+ influx in coronary smooth muscle cells by 31% and increased single cell phosphotyrosine by 95%.
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