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  • Title: Regulation of cardiac calcium channel current and contractile activity by the dihydropyridine Bay K 8644 is voltage-dependent.
    Author: Sanguinetti MC, Kass RS.
    Journal: J Mol Cell Cardiol; 1984 Jul; 16(7):667-70. PubMed ID: 6206231.
    Abstract:
    Pharmacological studies have provided considerable information about the molecular structure of ion channels in the membranes of excitable cells. Two classes of drugs, the local anesthetics and the biotoxins, have been used to study sodium channels in nerve, skeletal muscle, and cardiac cells, and tetraethylammonium ion and many of its derivatives have provided structural information about potassium channels in nerve. More recently, organic compounds that block calcium channels (calcium channel antagonists) have begun to be used to probe calcium channels in cardiac and smooth muscle cells (see). One group of calcium channel blockers, the dihydropyridines, has provided considerable information on the structure and function of these channels on the basis of electrophysiological and binding studies. Slight modification of the structure of one of these dihydropyridines, nifedipine, has led to the discovery of a group of compounds that are presumed to act by increasing the influx of Ca2+ into cardiac and smooth muscle cells. One of these novel compounds, Bay K 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5 carboxylate) has been reported to act at the same receptor site as the calcium channel antagonist nifedipine, but enhances contractile activity of the perfused heart and aortic strips. Because activation of contraction in cardiac muscle is closely linked to calcium entry via voltage-dependent calcium channels (see for review) these results suggested that Bay K 8644 might act on these channels.
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