FEBS Letters · 1983 · 95 citations · 9 references
MedicineBiochemistryPharmacologyIon Channel BiophysicsMolecular PharmacologyPharmacodynamicsCalcium SignalingIon Channel PharmacologyIon Channel PhysiologyIon Channel RegulationIon ChannelsLigand BindingCalcium Channel PharmacodynamicsCalcium Channel PharmacologyCalcium Channel PhysiologyCalcium Signaling In Muscle CellsDiltiazem TherapyDrug Binding To Ion ChannelsLigand-gated Calcium ChannelsVoltage-gated Calcium Channels
The binding of the Ca2+-channel blocker d-cis-[3H]diltiazem to guinea pig skeletal muscle microsomes is temperature-dependent. At 2 degrees C the KD is 39 nM and Bmax is 11 pmol/mg protein. The binding is fully reversible (K -1 = 0.02 min -1). The binding sites discriminate between the diastereoisomers l- and d-cis-diltiazem, reconize verapamil, gallopamil and tiapamil, and are sensitive to La3+-inhibition. At 30 degrees C the KD is 37 nM and the Bmax is 2.9 pmol/mg protein. D-cis-diltiazem-labelling is regulated by the 1,4-dihydropyridine Ca2+-channel blockers and a novel Ca2+-channel activator in a temperature-dependent manner. At 30 degrees C an enhancement of d-cis-diltiazem binding by the channel blockers is observed. This is attributed to a Bmax increase. EC50-values for enhancement and the maximal enhancement differ for the individual 1,4-dihydropyridines. At 2 degrees C 1,4-dihydropyridines inhibit d-cis-[3H]diltiazem binding. This is attributed to a Bmax decrease. We have directly labelled one of the drug receptor sites within the Ca2+-channel which can allosterically interact with the 1,4-dihydropyridine binding sites.
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Novel dihydropyridines with positive inotropic action through activation of Ca2+ channels
Matthias Schramm, G. Thomas, R. Towart et al. · Nature · 1983 · 1K citations
Taku Nagao, Masanori Sato, Yoshio Iwasawa et al. · The Japanese Journal of Pharmacology · 1972 · 78 citations · Full text