Sunano S, Shimada T, Shimamura K
Nihon Heikatsukin Gakkai Zasshi. 1985 Apr;21(2):95-105. doi: 10.1540/jsmr1965.21.95.
Effects of sodium vanadate on electrical and mechanical activities of smooth muscle of the guinea-pig vas deferens were investigated. Sodium vanadate of concentrations higher than 5 X 10(-6) M caused an elevation of basal tension and, at concentrations higher than 5 X 10(-4) M, initiated spontaneous contractions. These effects were not blocked by treatments with reserpine, tetrodotoxin or phentolamine. Treatment with ouabain also did not block the tension development by sodium vanadate. Sodium vanadate caused slight depolarization of membrane and potentiated spike activities. The phasic contraction of potassium contracture was potentiated by sodium vanadate in a similar manner to pretreatment with 15 mM K+ or with ouabain, both treatments occasioning slight depolarization. Sodium vanadate also caused tension development in K-depolarized preparetions. Contrastingly, drug-induced contractions were not significantly affected by sodium vanadate. It is suggested that sodium vanadate acts directly on smooth muscles and causes tension development without relation to Na, K-ATPase activity. Changes in the membrane electrical activities may be part of the cause of contraction. However, it can also initiate tension development without membrane potential changes, presumably acting on intracellular Ca binding sites.
研究了钒酸钠对豚鼠输精管平滑肌电活动和机械活动的影响。浓度高于5×10⁻⁶M的钒酸钠可引起基础张力升高，而浓度高于5×10⁻⁴M时可引发自发收缩。利血平、河豚毒素或酚妥拉明处理均不能阻断这些效应。哇巴因处理也不能阻断钒酸钠引起的张力增加。钒酸钠可引起膜轻微去极化并增强锋电位活动。钒酸钠以类似于用15 mM K⁺或哇巴因预处理的方式增强钾挛缩的相性收缩，这两种处理均引起轻微去极化。钒酸钠也可在钾去极化标本中引起张力增加。相反，药物诱导的收缩不受钒酸钠的显著影响。提示钒酸钠直接作用于平滑肌并引起张力增加，与钠钾ATP酶活性无关。膜电活动的变化可能是收缩的部分原因。然而，它也可在无膜电位变化的情况下引发张力增加，推测是作用于细胞内钙结合位点。
