In the present study, the author characterized Ca
2+ entry pathways in cultured rat aortic smooth muscle cells (SMCs) by measuring the influx of extracellularly added
45Ca
2+ or Mn
2+ and by measuring the extracellular Ca
2+-induced increase in [Ca
2+]
i under conditions in which removal of cytosolic Ca
2+ was inhibited. Ca
2+ influx into resting SMCs was inhibited by DHP Ca
2+ antagonist PN200-110 and hyperpolarization, and was activated by the DHP Ca
2+ agonist BayK8644. Endothelin-1 and PMA suppressed Ca
2+-channel activity. The suppressing effects of Endothelin-1 and PMA disappeared when the cells were pretreated with staurosporine, an inhibitor of C kinase. These findings indicate that activation of C kinase causes sustained inhibition of Ca
2+-channel activity. DHP-insensitive Ca
2+-and/or Mn
2+-influx pathways exist in rat aortic SMCs for Mn
2+ influx.
These DHP-resistant pathways are unaffected by endothelin-1, PMA or elevated [Ca
2+]
i. SR constitutes a large Ca
2+ pool in SMCs. Thus, the overall rate of
45Ca
2+ label equilibration in SMCs depends not only on the efficiency of transsarcolemmal flux but on the size and the Ca
2+ pumping activity of the SR Ca
2+ pool.
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