1. It has been suggested that the toxic effect of toxoflavin (TXF) produced by Pseudomonas cocovenenas is mainly due to the impairment of electron transfer of the mitochondrial respiratory chain. However, the cardiovascular effect of TXF is unknown. In the present study, the effect of TXF on the isometric contraction of rat isolated tail artery strips and the underlying mechanisms were investigated. 2. The basal force of the tissues was not affected by the toxin. However, the application of TXF before or during KCl (60 mM) stimulation potentiated KCl-induced vasocontraction, specifically the tonic phase of the contraction. 3. When the vessel strips were precontracted with phenylephrine (Phe), TXF further enhanced the tonic contraction of the tissue. Pretreatment of tissues with TXF also potentiated subsequent vasocontraction induced by Phe. The vasocontractor effects of TXF and Phe, however, were not additive. 4. The vascular effect of TXF was not mediated by oxygen-derived free radicals since catalase and SOD did not affect TXF-enhanced vasocontraction. In contrast, the vasocontractor effect of TXF was dependent on extracellular Ca2+ and abolished by nifedipine (a Ca2+ antagonist). TXF also had no effect on caffeine- or U46619-induced vasocontraction. 5. It is suggested that TXF may potentially contract blood vessels via its effect on Ca2+ channels. This effect of TXF depends on the contractile status of the vascular tissues.
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