Kaiser L, Sparks H V
Circ Shock. 1986;18(2):109-14.
When blood flow in a large artery is increased the vessel dilates. This flow-dependent dilation requires endothelial cells, and is not mediated by an ascending message from the microcirculation or a myogenic mechanism. Adrenergic, cholinergic, or ganglionic blockade does not alter the dilation response. Inhibition of cyclo-oxygenase by indomethacin has no effect, but inhibition of both lipoxygenase and cyclo-oxygenase by 5,8,11,14-eicosatetraynoic acid (ETYA) inhibits the dilation and shifts the acetylcholine dose response curve to the right. Inhibition of guanylate cyclase by methylene blue blocks the dilation response and shifts the acetylcholine dose response curve to the right. This suggests that both cyclic GMP and a nonprostaglandin metabolite of arachidonic acid are involved in the dilation response to increased flow. We propose that increased blood flow initiates an initial response, which results in endothelial cell production and release of a nonprostaglandin metabolite of arachidonic acid. This metabolite stimulates vascular smooth muscle guanylate cyclase, leading to increased cyclic GMP and vasodilation.
当大动脉中的血流量增加时，血管会扩张。这种流量依赖性扩张需要内皮细胞，并非由微循环传来的上行信号或肌源性机制介导。肾上腺素能、胆碱能或神经节阻断均不改变扩张反应。吲哚美辛抑制环氧化酶没有作用，但5,8,11,14-二十碳四烯酸（ETYA）同时抑制脂氧化酶和环氧化酶会抑制扩张，并使乙酰胆碱剂量反应曲线右移。亚甲蓝抑制鸟苷酸环化酶会阻断扩张反应，并使乙酰胆碱剂量反应曲线右移。这表明环磷酸鸟苷（cGMP）和花生四烯酸的非前列腺素代谢产物均参与了对血流量增加的扩张反应。我们提出，血流量增加引发初始反应，导致内皮细胞产生并释放花生四烯酸的非前列腺素代谢产物。这种代谢产物刺激血管平滑肌鸟苷酸环化酶，导致cGMP增加和血管舒张。
