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• W820637579 abstract "The ability of N-n-butyl haloperidol iodide (F 2 ) to cause vasodilation, and thereby produce a cardioprotective effect, has been well documented. The aim of this study was to investigate whether F 2 might act as a Ca 2+ antagonist. Myocytes were obtained from rat heart, and the whole-cell patch-clamp technique was used to record Ca 2+ current. Laser scanning confocal microscopy was used to measure intracellular free calcium ([Ca 2+ ] i ). The results obtained from this study demonstrate that F 2 reduced calcium current (I Ca ) in a concentration-dependent manner with an IC 50 of 1.19 µmol/L, upshifted the current-voltage curve of I Ca , shifted the inactivation kinetics of I Ca leftward, and slowed down the recovery of I Ca from inactivation. F 2 decreased the fluorescent intensity of [Ca 2+ ] i elevation induced by KCl with an IC 50 of 1.61 µmol/L, and had no effects on the intracellular calcium release induced by caffeine and inositol-1,4,5-trisphosphate. These findings indicate that F 2 may act as a calcium antagonist, which could account for its cardiovascular benefits." @default.
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• W820637579 date "2007-04-01" @default.
• W820637579 modified "2023-10-18" @default.
• W820637579 title "Effects of N-n-butyl haloperidol iodide on L-type calcium channels and intracellular free calcium in rat ventricular myocytesThis paper is one of a selection of papers in this Special Issue, entitled International Symposium on Recent Advances in Molecular, Clinical, and Social Medicine, and has undergone the Journal's usual peer-review process." @default.
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• W820637579 doi "https://doi.org/10.1139/o07-012" @default.
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