Effects of antimycin A on vascular and intestinal smooth muscle contraction and calcium movements

The effects of antimycin A on smooth muscle preparations of guinea-pig taenia coli and rabbit aorta were investigated. In guinea-pig taenia coli, antimycin A inhibited the sustained phase but had less effect on the transient phase of K-induced contraction. The inhibitory effect of antimycin A became less in the presence of high concentration (40 mM) of glucose under hypoxia whereas antimycin A strongly inhibited both transient and sustained phase of K-induced contraction in the absence of glucose. Antimycin A inhibited the K-induced increase in cellular Ca content but not the increased rate of Ca uptake at the concentration needed to inhibit the K-induced contraction in taenia coli. In rabbit aorta, antimycin A inhibited the K-induced contraction only in the absence of glucose. Antimycin A inhibited the norepinephrine-induced contraction in aorta and this inhibitory effect was not observed in the presence of 40 mM glucose under hypoxia. Antimycin A inhibited the K-induced increase in cellular Ca content at a concentration without any effect on the K-induced contraction in aorta. On the other hand, the K-induced increase in the rate of Ca uptake was not inhibited by antimycin A. Antimycin A reduced oxygen consumption of resting and K-stimulated muscle, and decreased tissue ATP content in high K solution in taenia coli and aorta. It is concluded that antimycin A inhibits mitochondrial function in both guinea-pig taenia coli and rabbit aorta, leading to an inhibition of the K-induced sustained contraction in taenia and norepinephrine-induced contraction in aorta. Antimycin A does not seem to inhibit K-stimulated Ca influx; this agent inhibits only K-induced increase in cellular Ca content, which may represent mitochondrial Ca accumulation.