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 stimulus; while CaV1s require a strong depolarization (~ +40 mV) to perform, a much weaker pulse (~ -40 mV) is sufficient to activate CaV3s.
Ca2+ channel blockers (CCBs) are a diverse class of pharmaceutical agents, usually targeted at CaV1s, of which dihydropyridines (DHPs) constitute a major subgroup. Inhibitors of Ca2+-mediated smooth muscle contractions, CCBs produce vasodilation, thus therapeutically managing hypertension and coronary heart disease. Additionally, benidipine is known to be an endothelium protectant as well as an antioxidant.
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 channels; 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-lasting.
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