Felodipine actions on vascular muscle Ca2+ channels.
Felodipine is a potent, but relatively slow, relaxation agent in rat caudal artery, decreasing 30 mM K+ contractions by 39% at a concentration of 1 nM and 88% at 10 nM. Membrane potential at rest was unchanged, but 10 nM felodipine caused a 5 mV hyperpolarization of vascular muscle cells previously depolarized by 30 mM K+. Felodipine selectively decreased the sustained, but not the transient, type of calcium current in a whole-cell voltage clamp of azygos venous muscle cells. Relaxation by felodipine was additive to that caused by 10 microM trifluoperazine, a calmodulin antagonist, arguing against an action of felodipine via calmodulin. The vascular muscle relaxant effects of felodipine appear to be explainable by blockade of the sustained type of calcium channels.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D004347:Drug Interactions; D015736:Felodipine; D007473:Ion Channels / Q000187:drug effects* / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009568:Nitrendipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D014268:Trifluoperazine / Q000494:pharmacology
D007473:Ion Channels; D014268:Trifluoperazine; D009568:Nitrendipine; D015736:Felodipine; D002118:Calcium