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.