Overview
- Furukawa, T. et al. (1999) J. Pharmacol. Exp. Ther. 291, 464.
Alomone Labs Benidipine hydrochloride inhibits T- and L-type voltage-gated Ca2+ currents expressed in Xenopus oocytes.A. Time course of CaV3.1 (T-type) current reversible inhibition by increasing concentrations of Benidipine hydrochloride (#B-120). Currents were elicited by application of voltage ramps from a holding potential of -100 mV to +60 mV (40 msec). B. Superimposed example traces of current response to voltage ramps before and during perfusion of 10 and 50 µM Benidipine hydrochloride as indicated. C. Time course of CaV1.2/α2-δ1/β2a (L-type) current inhibition 10 µM of Benidipine hydrochloride. Currents were elicited by application of voltage steps from a holding potential of -100 mV to 0 mV (100 msec). D. Superimposed example traces of current responses before and during perfusion of 10 µM Benidipine hydrochloride as indicated.
- Furukawa, T. et al. (1999) J. Pharmacol. Exp. Ther. 291, 464.
- Minor, D.L. and Findeisen, F. et al. (2010) Channels (Austin) 4, 459.
- Godfraind, T. (2005) Philos. Trans. R. Soc. Lond. B. Biol. Sci. 360, 2259.
- Clunn, G.F. et al. (2010) Int. J. Cardiol. 139, 2.
- Yao, K. et al. (2006) J. Pharmacol. Sci. 100, 243.
- Kitakaze, M. et al. (1999) Cardiovasc. Drug Rev. 17, 1.
Both L-type (CaV1) and T-type (CaV3) voltage-gated Ca2+ channels are large (~0.5 MDa), transmembrane proteins which control the cellular influx of Ca2+ in response to electrical stimuli. While CaV1s require a strong depolarization (~+40 mV) to perform, a much weaker pulse (~-40 mV) is sufficient to activate CaV3s1.
Ca2+ channel blockers (CCBs) are a diverse class of pharmaceutical agents, usually targeted at CaV1s, of which dihydropyridines (DHPs) constitute a major subgroup2,3. Inhibitors of Ca2+-mediated smooth muscle contractions, CCBs produce vasodilation, thus therapeutically managing hypertension and coronary heart disease2. Additionally, benidipine is known to be an endothelium protectant as well as an antioxidant4,5.
A DHP derivative, benidipine hydrochloride acts as a triple-channel (CaV1, CaV2 and CaV3) blocker and is characterized by slow onset of action and high affinity for the binding sites of its target channels4; with a Ki value of 0.08-0.13 nmol/L benidipine's cell-membrane association is considerably greater than other DHPs, and a dissociation rate which is 9 times slower than that of nifedipine makes it distinguishably long-lasting4,5.
Benidipine hydrochloride (#B-120) is a highly pure, synthetic, and biologically active compound.
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