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Effects of N-n-butyl haloperidol iodide on L-type calcium channels and intracellular free calcium in rat ventricular myocytes.
Biochem Cell Biol. 2007 Apr; 85(2):182-8.BC

Abstract

The ability of N-n-butyl haloperidol iodide (F2) to cause vasodilation, and thereby produce a cardioprotective effect, has been well documented. The aim of this study was to investigate whether F2 might act as a Ca2+ antagonist. Myocytes were obtained from rat heart, and the whole-cell patch-clamp technique was used to record Ca2+ current. Laser scanning confocal microscopy was used to measure intracellular free calcium ([Ca2+]i). The results obtained from this study demonstrate that F2 reduced calcium current (ICa) in a concentration-dependent manner with an IC50 of 1.19 micromol/L, upshifted the current-voltage curve of ICa, shifted the inactivation kinetics of ICa leftward, and slowed down the recovery of ICa from inactivation. F2 decreased the fluorescent intensity of [Ca2+]i elevation induced by KCl with an IC50 of 1.61 micromol/L, and had no effects on the intracellular calcium release induced by caffeine and inositol-1,4,5-trisphosphate. These findings indicate that F2 may act as a calcium antagonist, which could account for its cardiovascular benefits.

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Authors+Show Affiliations

Huang Z
Department of Pharmacology, Shantou University Medical College, Xinling Road 22, Shantou 515041, China.
Shi G
No affiliation info available
Gao F
No affiliation info available
Zhang Y
No affiliation info available
Liu X
No affiliation info available
Christopher TA
No affiliation info available
Lopez B
No affiliation info available
Ma X
No affiliation info available

MeSH

AnimalsCaffeineCalciumCalcium Channels, L-TypeCells, CulturedCentral Nervous System StimulantsHaloperidolHeart VentriclesInositol 1,4,5-TrisphosphateMyocytes, CardiacRatsRats, Sprague-DawleyVasodilation

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17534398

Citation

Huang, Zhanqin, et al. "Effects of N-n-butyl Haloperidol Iodide On L-type Calcium Channels and Intracellular Free Calcium in Rat Ventricular Myocytes." Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire, vol. 85, no. 2, 2007, pp. 182-8.
Huang Z, Shi G, Gao F, et al. Effects of N-n-butyl haloperidol iodide on L-type calcium channels and intracellular free calcium in rat ventricular myocytes. Biochem Cell Biol. 2007;85(2):182-8.
Huang, Z., Shi, G., Gao, F., Zhang, Y., Liu, X., Christopher, T. A., Lopez, B., & Ma, X. (2007). Effects of N-n-butyl haloperidol iodide on L-type calcium channels and intracellular free calcium in rat ventricular myocytes. Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire, 85(2), 182-8.
Huang Z, et al. Effects of N-n-butyl Haloperidol Iodide On L-type Calcium Channels and Intracellular Free Calcium in Rat Ventricular Myocytes. Biochem Cell Biol. 2007;85(2):182-8. PubMed PMID: 17534398.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of N-n-butyl haloperidol iodide on L-type calcium channels and intracellular free calcium in rat ventricular myocytes. AU - Huang,Zhanqin, AU - Shi,Ganggang, AU - Gao,Fenfei, AU - Zhang,Yanmei, AU - Liu,Xingping, AU - Christopher,Theodore A, AU - Lopez,Bernard, AU - Ma,Xinliang, PY - 2007/5/31/pubmed PY - 2007/8/3/medline PY - 2007/5/31/entrez SP - 182 EP - 8 JF - Biochemistry and cell biology = Biochimie et biologie cellulaire JO - Biochem Cell Biol VL - 85 IS - 2 N2 - The ability of N-n-butyl haloperidol iodide (F2) to cause vasodilation, and thereby produce a cardioprotective effect, has been well documented. The aim of this study was to investigate whether F2 might act as a Ca2+ antagonist. Myocytes were obtained from rat heart, and the whole-cell patch-clamp technique was used to record Ca2+ current. Laser scanning confocal microscopy was used to measure intracellular free calcium ([Ca2+]i). The results obtained from this study demonstrate that F2 reduced calcium current (ICa) in a concentration-dependent manner with an IC50 of 1.19 micromol/L, upshifted the current-voltage curve of ICa, shifted the inactivation kinetics of ICa leftward, and slowed down the recovery of ICa from inactivation. F2 decreased the fluorescent intensity of [Ca2+]i elevation induced by KCl with an IC50 of 1.61 micromol/L, and had no effects on the intracellular calcium release induced by caffeine and inositol-1,4,5-trisphosphate. These findings indicate that F2 may act as a calcium antagonist, which could account for its cardiovascular benefits. SN - 0829-8211 UR - https://www.unboundmedicine.com/medline/citation/17534398/Effects_of_N_n_butyl_haloperidol_iodide_on_L_type_calcium_channels_and_intracellular_free_calcium_in_rat_ventricular_myocytes_ L2 - https://cdnsciencepub.com/doi/10.1139/O07-012?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -