Bay K8644 differentiates between potential and receptor operated Ca2+ channels.
Bay K8644 increased unidirectional Ca2+ influx and produced tension development in rabbit aorta. Both responses could be evoked in the tissue maximally stimulated with norepinephrine. When the arterial rings were maximally activated by high K+ depolarization, Bay K8644 was without effect. The tension evoked by high K+ and Bay K8644 was more sensitive to the dihydropyridine Ca2+ antagonist PY108-068 than norepinephrine induced tension. These results indicate that Bay K8644 activates only potential operated Ca2+ channels which are opened by high K+ depolarization.
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D000818:Animals; D001011:Aorta / Q000187:drug effects; D015220:Calcium Channels; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects* / Q000502:physiology; D008564:Membrane Potentials; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011817:Rabbits; D011978:Receptors, Nicotinic / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects
D015220:Calcium Channels; D007473:Ion Channels; D011978:Receptors, Nicotinic; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine; D009638:Norepinephrine