NDLI: Clotrimazole inhibits the recombinant human cardiac L-type Ca2+ channel α1C subunit

Content Provider	PubMed Central
Author	Ball, S. G. Peers, C. Fearon, I. M.
Copyright Year	2000
Abstract	Clotrimazole (CLT) is an antimycotic agent with a potential role in the treatment of cancer. Whole-cell patch clamp recordings and Fura-2 AM fluorescence measurements were used to investigate the inhibition by CLT of recombinant human cardiac L-type Ca2+ channel α1C subunits, stably expressed in human embryonic kidney (HEK 293) cells. CLT (100 nmol l−1 to 25 μmol l−1) reduced Ca2+ channel currents in a concentration-dependent manner. Inhibition was neither use- or voltage-dependent. The effects of CLT were rapid and maximal effects were attained within 3 min. Application of CLT also caused an acceleration of apparent Ca2+ channel current inactivation. Basal current density and the degree of inhibition due to CLT were not significantly altered by pretreating cells with 3 mmol l−1 1-aminobenzotriazole for 1 h, or by dialysing cells for 10 min with 2 mmol l−1 α-napthoflavone via the patch pipette, suggesting that the inhibitory action of CLT was not due to inhibition of cytochrome P-450. CLT (10 μmol l−1) did not influence [Ca2+]i, as determined by Fura-2 AM fluorescence measurements. Dialysing cells for 10 min with the non-specific serine/threonine kinase inhibitor H-7 (10 μmol l−1) was without effect on basal current density or on the inhibitory response to 10 μmol l−1 CLT, indicating that CLT is not acting via an indirect effect on these kinases. These data suggest that CLT exerts a direct blocking effect on the α1C subunit at therapeutic concentrations. This effect may explain the abbreviation of the action potential duration by CLT observed in cardiac myocytes.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0703106
Ending Page	554
Page Count	8
Starting Page	547
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	3
Volume Number	129
Language	English
Publisher Date	2000-02-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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