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The glucocorticoid hydrocortisone (HC), applied for up to 2 weeks to either aneurally or innervated cultured human muscle, produced 2-fold increase of the number of dihydropyridine ([3H]PN200-110) binding sites. The K(+)-induced, nifedipine-inhibited Ca2+ uptake was increased 40%. The effect of HC was concentration- and time-dependent. [3H]PN200-110 affinity for its receptor was not affected by HC treatment. HC did not exert significant influence on the total amount of protein, CK activity, and the number of myotubes. These results indicate that voltage-dependent L-type Ca2+ channel expression in human muscle is regulated by glucocorticoid.
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