Tran N N, Robert A, Atkinson J, Capdeville-Atkinson C
Laboratoire de Pharmacologie Cardio-vasculaire, Faculté de Pharmacie, Université Henri Poincaré-Nancy 1, France.
Am J Physiol. 1997 Sep;273(3 Pt 1):C834-42. doi: 10.1152/ajpcell.1997.273.3.C834.
We investigated the possibility that the inhibition of oxidative phosphorylation in vascular smooth muscle attenuates norepinephrine- or KCl-evoked vasoconstriction with no change in mobilization of intracellular calcium concentration ([Ca2+]i). Experiments were performed in perfused segments of the rat tail artery loaded with the intracellular calcium dye fura 2, in the absence and presence of dinitrophenol or sodium cyanide; inhibition of oxidative phosphorylation was evaluated from the fall in intracellular ATP levels. The metabolic inhibitors reduced vasoconstriction with no change in [Ca2+]i handling, suggesting that 1) inhibition of oxidative phosphorylation attenuates vasoconstriction via a mechanism downstream of [Ca2+]i, and 2) [Ca2+]i homeostasis (both increases and decreases in [Ca2+]i) can be maintained in the presence of inhibitors of oxidative phosphorylation.
我们研究了血管平滑肌中氧化磷酸化的抑制作用是否能减弱去甲肾上腺素或氯化钾诱发的血管收缩,而细胞内钙浓度([Ca2+]i)的动员却没有变化。实验在灌注的大鼠尾动脉节段中进行,该节段加载了细胞内钙染料fura 2,分别在不存在和存在二硝基苯酚或氰化钠的情况下进行;通过细胞内ATP水平的下降来评估氧化磷酸化的抑制作用。代谢抑制剂减少了血管收缩,而[Ca2+]i的处理没有变化,这表明:1)氧化磷酸化的抑制通过[Ca2+]i下游的机制减弱血管收缩;2)在存在氧化磷酸化抑制剂的情况下,可以维持[Ca2+]i的稳态([Ca2+]i的增加和减少)。