Overview
- Arun, K.H. et al. (2005) Cardiovasc. Res. 65, 374.
Alomone Labs Lercanidipine hydrochloride inhibits L-type voltage-gated Ca2+ currents expressed in Xenopus oocytes.A. Time course of CaV1.2/α2-δ1/β2a current inhibition by 10 and 30 µM Lercanidipine hydrochloride (#L-115). Currents were elicited by application of voltage steps from a holding potential of -80 mV to 0 mV (100 msec). B. Superimposed example traces of current responses before and during perfusion of 10 and 30 µM Lercanidipine hydrochloride (as indicated).
- Bers, D.M. et al. (1999) Cardiovasc. Res. 42, 339.
- Hockerman, G.H. et al. (2000) Annu. Rev. Pharmacol. Toxicol. 37, 361.
- Hair, P.I. et al. (2007) Drugs 67, 95.
- Rimoldi, E. et al. (1994) Acta. Therap. 20, 23.
- Agrawal, R. et al. (2006) J. Hypertens. 24,185.
Ca2+ influx via voltage-dependent L-type Ca2+ channels (CaV1.2) found in cardiac and vascular smooth muscle initiates contraction and contributes to timing of the cardiac action potential1. CaV1.2 is sensitive to block by three distinct classes of small-molecule drugs: dihydropyridines (DHPs), phenylalkylamines (PAAs), and benzothiazepines (BZPs)2.
Lercanidipine hydrochloride is antihypertensive drug structurally related to dihydropyridine (DHP) calcium channel blockers3. It is similar to other pheripheral vasodialators. It inhibits the influx of extracellular Ca2+ across the myocardial and vascular smooth muscle cell membranes4. The effect of lercanidipine hydrochloride has also successfully evaluated in severe or resistant hypertension, elderly subjects, and diabetics5.
Lercanidipine hydrochloride (#L-115) is a highly pure, synthetic, and biologically active compound.
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