Mikkelsen E
Br J Pharmacol. 1985 Jun;85(2):383-5. doi: 10.1111/j.1476-5381.1985.tb08872.x.
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. The results are consistent with the conclusion that in rat portal vein, Bay K 8644 increases the entry of extracellular Ca by a mechanism antagonistic to that of nifedipine and in high concentration has a Ca-entry blocking effect.
在大鼠离体门静脉中,Bay K 8644(甲基-1,4-二氢-2,6-二甲基-3-硝基-4-(2-三氟甲基苯基)吡啶-5-羧酸酯)在低浓度而非高浓度时增加自发机械活性。Bay K 8644诱导的自发机械活性增加在无钙培养基中消失,并通过重新添加钙而恢复。硝苯地平消除了Bay K 8644对自发机械活性的增强作用;硝苯地平的这种作用可通过进一步增加Bay K 8644的浓度而消除。结果与以下结论一致:在大鼠门静脉中,Bay K 8644通过一种与硝苯地平相反的机制增加细胞外钙的内流,且在高浓度时有钙内流阻断作用。