Nasu T, Sasaki M
Department of Veterinary Pharmacology, Faculty of Agriculture, Yamaguchi University, Japan.
J Pharm Pharmacol. 1998 Mar;50(3):311-5. doi: 10.1111/j.2042-7158.1998.tb06866.x.
We have studied the effects of Mn2+ on the contractile response induced by Bay K 8644, a dihydropyridine Ca2+ agonist, on guinea-pig taenia coli. Mn2+ (5 mM) completely inhibited Bay K 8644 (10(-6) M)-induced rhythmic contraction and contracture to baseline values in normal Ca2+ medium; thereafter, the contraction progressively increased to about 90% of the K+ (60 mM)-induced tonic response. In Ca2+-free medium in the presence of Bay K 8644 Mn2+ also evoked contraction and a concomitant increase in Mn2+ influx into the cytoplasm. These results suggest that during the opening of voltage-dependent Ca2+ channels activated by Bay K 8644, Mn2+ can enter cytoplasm through the channels and induce contraction in taenia coli.
我们研究了锰离子（Mn2+）对豚鼠结肠带条上由二氢吡啶类钙离子激动剂Bay K 8644诱导的收缩反应的影响。在正常钙离子培养基中，5 mM的Mn2+可完全抑制10^(-6) M的Bay K 8644诱导的节律性收缩和挛缩，使其恢复到基线值；此后，收缩逐渐增加至约为60 mM钾离子诱导的强直反应的90%。在无钙离子培养基中，存在Bay K 8644时，Mn2+也可诱发收缩，并伴随Mn2+流入细胞质的增加。这些结果表明，在Bay K 8644激活电压依赖性钙离子通道开放期间，Mn2+可通过这些通道进入细胞质并诱导结肠带条收缩。
