Shimamura K, Sunano S
Research Institute of Hypertension, Kinki University, Osaka, Japan.
Naunyn Schmiedebergs Arch Pharmacol. 1988 Mar;337(3):347-53. doi: 10.1007/BF00168849.
The effects of vanadate on the mechanical and electrical activity of the rat portal vein were examined. Vanadate increased the height of the spontaneous contractions of the portal vein without affecting basal tension. This effect was not blocked by alpha-blockers or atropine. Vanadate did not exert any effect when the spontaneous contractions were abolished by high concentrations of verapamil or in the absence of Ca. Vanadate did not change the resting membrane potential of the smooth muscle cells of the vein, but it increased the rate of rise and the amplitude of the action potentials and the number of action potentials per burst. The intracellular Na content was increased slightly by vanadate. However, the effects of Na,K-pump inhibition by ouabain or K-removal were quite different from those of vanadate, and these procedures did not block the effect of vanadate, although they attenuated it. Vanadate also potentiated the K-contracture of the portal vein. These results indicate that vanadate increases the amplitude of the spontaneous contractions through an increase in the number of action potentials per burst which underly the contraction. These effects are not mediated by intrinsic nerve excitation or inhibition of Na,K pump activity. The facilitation of Ca entry through the voltage dependent Ca channel may be the main cause of the effect of vanadate on mechanical activity.
研究了钒酸盐对大鼠门静脉机械和电活动的影响。钒酸盐增加了门静脉自发收缩的幅度，而不影响基础张力。这种作用不受α受体阻滞剂或阿托品的阻断。当高浓度维拉帕米消除自发收缩或在无钙条件下，钒酸盐没有任何作用。钒酸盐不改变静脉平滑肌细胞的静息膜电位，但增加了动作电位的上升速率、幅度以及每阵发放动作电位的数量。钒酸盐使细胞内钠含量略有增加。然而，哇巴因抑制钠钾泵或去除钾的作用与钒酸盐的作用有很大不同，这些操作虽减弱但不阻断钒酸盐的作用。钒酸盐还增强了门静脉的钾挛缩。这些结果表明，钒酸盐通过增加每阵发放动作电位的数量来增加自发收缩的幅度，而这些动作电位是收缩的基础。这些作用不是由内在神经兴奋或钠钾泵活性抑制介导。通过电压依赖性钙通道促进钙内流可能是钒酸盐对机械活动产生作用的主要原因。
