This preclinical study demonstrates that protein kinase C activation inhibits calcium channel activity in rat aortic smooth muscle cells, while DHP-insensitive calcium entry pathways remain unaffected.
Reversible PKC inhibition of Ca2+ channels in rat cells; hypothesis-generating for endothelin signaling in vascular disease.
In the present study, the author characterized Ca2+ entry pathways in cultured rat aortic smooth muscle cells (SMCs) by measuring the influx of extracellularly added 45Ca2+ or Mn2+ and by measuring the extracellular Ca2+-induced increase in [Ca2+] i under conditions in which removal of cytosolic Ca2+ was inhibited. Ca2+ influx into resting SMCs was inhibited by DHP Ca2+ antagonist PN200-110 and hyperpolarization, and was activated by the DHP Ca2+ agonist BayK8644. Endothelin-1 and PMA suppressed Ca2+-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 Ca2+-channel activity. DHP-insensitive Ca2+-and/or Mn2+-influx pathways exist in rat aortic SMCs for Mn2+ influx.These DHP-resistant pathways are unaffected by endothelin-1, PMA or elevated [Ca2+] i. SR constitutes a large Ca2+ pool in SMCs. Thus, the overall rate of 45Ca2+ label equilibration in SMCs depends not only on the efficiency of transsarcolemmal flux but on the size and the Ca2+ pumping activity of the SR Ca2+ pool.
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Nobuhiro Ohshima (1994) studied this question.
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