Stirrat Alison, Nelli Silvia, McGuckin Alicia, Ho Vivian Wing Man, Wilson William S, Martin William
Division of Neuroscience and Biomedical Systems, Institute of Biomedical and Life Sciences, West Medical Building, University of Glasgow, Glasgow G12 8QQ, Scotland, UK.
Eur J Pharmacol. 2006 Mar 18;534(1-3):152-8. doi: 10.1016/j.ejphar.2006.01.029.
Ascorbate blocks agonist-induced, endothelium-derived hyperpolarizing factor (EDHF)-mediated vasodilatation in the bovine perfused ciliary artery and this is associated with a rise in perfusion pressure. We now report the origins of this ascorbate-induced rise in perfusion pressure. In segments of ciliary artery perfused at 2.5 ml/min, the addition of ascorbate (10-150 microM) enhanced U46619-induced perfusion pressure. Ascorbate produced no enhancement in the absence of U46619, suggesting that its effects resulted not from a constrictor action but through removal of a tonic vasodilator influence. Experiments revealed the endothelial source of this vasodilator influence, and EDHF, but not nitric oxide or prostanoids, appeared to be involved. The ascorbate-induced enhancement of vasoconstrictor tone was not seen in a static myograph or in segments perfused at low rates of flow, but was seen at flow rates of 2.5 ml(-1) and above. We conclude that ascorbate augments vasoconstrictor tone through inhibition of flow-induced EDHF activity.
抗坏血酸盐可阻断激动剂诱导的、内皮衍生超极化因子(EDHF)介导的牛灌注睫状动脉血管舒张,且这与灌注压升高有关。我们现在报告这种抗坏血酸盐诱导的灌注压升高的起源。在以2.5毫升/分钟灌注的睫状动脉节段中,加入抗坏血酸盐(10 - 150微摩尔)可增强U46619诱导的灌注压。在没有U46619的情况下,抗坏血酸盐不会产生增强作用,这表明其作用并非源于收缩作用,而是通过消除一种持续性血管舒张影响。实验揭示了这种血管舒张影响的内皮来源,且似乎涉及EDHF,而非一氧化氮或前列腺素。抗坏血酸盐诱导的血管收缩张力增强在静态肌动描记器中或低流速灌注的节段中未观察到,但在流速为2.5毫升/分钟及以上时可见。我们得出结论,抗坏血酸盐通过抑制血流诱导的EDHF活性增强血管收缩张力。