Inhibitory Mechanism of Monensin on High K⁺-Induced Contraction in Guniea-Pig Urinary Bladder

抄録

In this study, we examined the inhibitory mechanism of monensin on high K⁺-induced contraction in guinea-pig urinary bladder. The relaxant effect of monensin (0.001 – 10 μM) was more potent than those of NaCN (100 μM – 1 mM) and forskolin (3 – 10 μM). Monensin (0.1 μM), NaCN (300 μM), or forskolin (10 μM) inhibited high K⁺-induced contraction without decreasing [Ca²⁺]_i level. Monensin and NaCN remarkably decreased creatine phosphate and ATP contents. Monensin and NaCN inhibited high K⁺-induced increases in flavoprotein fluorescence, which is involved in mitochondrial respiration. Forskolin increased cAMP content but monensin did not. Monensin increased Na⁺ content at 10 μM but not at 0.1 μM that induced maximum relaxation. In the α-toxin-permeabilized muscle, forskolin significantly inhibited the Ca²⁺-induced contraction, but monensin did not affect it. These results suggest that the relaxation mechanism of monensin in smooth muscle of urinary bladder may be an inhibition of oxidative metabolism.