Abstract
In isolated portal veins from rats, Bay K 8644 (methyl-1, 4-dihydro-2, 6-dimethyl-3-nitro-4 (2-trifluoromethyl-phenyl)pyridine-5-carboxylate) increased the spontaneous mechanical activity in low but not in high concentrations. The Bay K 8644-induced increase in spontaneous mechanical activity was abolished in Ca-free medium and restored by readdition of Ca. Nifedipine abolished the augmenting effect of Bay K 8644 on the spontaneous mechanical activity; this effect of nifedipine could be eliminated by further increasing the concentration of Bay K 8644. In the rat portal vein, Bay K 8644 evidently increases the entry of extracellular Ca by a mechanism antagonistic to that of nifedipine, and in high concentration has a Ca-entry blocking effect.