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首页> 外文期刊>American Journal of Physiology >Elucidation of the temporal relationship between endothelial-derived NO and EDHF in mesenteric vessels.
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Elucidation of the temporal relationship between endothelial-derived NO and EDHF in mesenteric vessels.

机译：阐明肠系膜血管中内皮源性NO和EDHF之间的时间关系。

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Although the endothelium co-generates both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), the relative contribution from each vasodilator is not clear. In studies where the endothelium is stimulated acutely, EDHF responses predominate in small arteries. However, the temporal relationship between endothelial-derived NO and EDHF over more prolonged periods is unclear but of major physiological importance. Here we have used a classical pharmacological approach to show that EDHF is released transiently compared with NO. Acetylcholine (3 x 10(-6) mol/l) dilated second- and/or third-order mesenteric arteries for prolonged periods of up to 1 h, an effect that was reversed fully and immediately by the subsequent addition of L-NAME (10(-3) mol/l) but not TRAM-34 (10(-6) mol/l) plus apamin (5 x 10(-7) mol/l). When vessels were pretreated with L-NAME, acetylcholine induced relatively transient dilator responses (declining over approximately 5 min), and vessels were sensitive to TRAM-34 plus apamin. When measured in parallel, the dilator effects of acetylcholine outlasted the smooth muscle hyperpolarization. However, in the presence of L-NAME, vasodilatation and hyperpolarization followed an identical time course. In vessels from NOSIII(-/-) mice, acetylcholine induced small but detectable dilator responses that were transient in duration and blocked by TRAM-34 plus apamin. EDHF responses in these mouse arteries were inhibited by an intracellular calcium blocker, TMB-8, and the phospholipase A(2) inhibitor AACOCF(3), suggesting a role for lipid metabolites. These data show for the first time that EDHF is released transiently, whereas endothelial-derived NO is released in a sustained manner.
机译：尽管内皮共同生成一氧化氮（NO）和内皮衍生的超极化因子（EDHF），但尚不清楚每种血管扩张剂的相对作用。在对内皮进行急性刺激的研究中，EDHF反应在小动脉中占主导地位。然而，内皮源NO和EDHF在更长的时间上的时间关系尚不清楚，但具有重要的生理意义。在这里，我们已经使用经典的药理学方法来证明EDHF与NO相比是瞬时释放的。乙酰胆碱（3 x 10（-6）mol / l）扩张肠系膜和/或三级肠系膜动脉长达1小时，随后通过添加L-NAME（ 10（-3）mol / l），但不包含TRAM-34（10（-6）mol / l）和木瓜蛋白酶（5 x 10（-7）mol / l）。当用L-NAME预处理血管时，乙酰胆碱会引起相对短暂的扩张反应（在大约5分钟内下降），并且血管对TRAM-34和Apapamin敏感。当平行测量时，乙酰胆碱的扩张作用比平滑肌超极化持久。但是，在存在L-NAME的情况下，血管舒张和超极化遵循相同的时间过程。在NOSIII（-/-）小鼠的血管中，乙酰胆碱诱导小的但可检测到的扩张反应，持续时间短暂，并被TRAM-34和木瓜蛋白酶阻断。在这些小鼠动脉中的EDHF反应被细胞内钙阻滞剂TMB-8和磷脂酶A（2）抑制剂AACOCF（3）抑制，表明脂质代谢物的作用。这些数据首次表明EDHF瞬时释放，而内皮源性NO则持续释放。

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