Mg 2 1 -induced endothelium-dependent relaxation of blood vessels and blood pressure lowering: role of NO
Mg 2 1 -induced endothelium-dependent relaxation of blood vessels and blood pressure lowering: role of NO
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发表时间：
2000
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通讯作者：
Zhi-wei Yang;A. Gebrewold;Maja Nowakowski;B. T. Altura;B. Altura
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作者：
Zhi-wei Yang;A. Gebrewold;Maja Nowakowski;B. T. Altura;B. Altura
Mg 2 1 诱导内皮依赖性血管舒张和血压降低：NO 的作用。是。 J.生理学。监管综合比较生理学。 278：R628–R639，2000。—体外细胞外 Mg 2 1 浓度（[Mg 2 1 ] 0 ）以浓度依赖性方式在大鼠主动脉中产生内皮依赖性和内皮非依赖性松弛。 Mg 2 1 对完整大鼠主动脉环（而非裸露大鼠主动脉环）的这些松弛作用可被 NG -单甲基-L 精氨酸 (L -NMMA)、N v -硝基-L -精氨酸甲酯 (L -NAME) 或亚甲蓝抑制。 L-NMMA和L-NAME的抑制作用可以被L-精氨酸部分逆转。 NG-硝基-L精氨酸和L-NMMA几乎完全抑制[Mg 2 1 ] 0 诱导的大鼠肠系膜小动脉和小静脉的体内扩张。用10 µM 1,2-双(2-氨基苯氧基)-乙烷-N,N,N 8 ,N 8 -四乙酸-AM去除内皮细胞中的细胞外Ca 2 1 浓度([Ca 2 1 ] 0 )或缓冲细胞内Ca 2 1 浓度，显着减弱了Mg 2 1 的松弛作用。 Mg 2 1 产生一氧化氮（NO），以浓度依赖性方式从完整的主动脉环中释放。 [Ca 2 1 ] 0 的去除减少了[Mg 2 1 ] 0 水平升高引起的NO释放增加。体内增加剂量（1-30 µM/分钟）的 MgSO 4 直接注入麻醉大鼠的股静脉，引起血清总 Mg 显着的浓度依赖性持续增加，并伴随动脉血压下降。在使用不同剂量的MgSO 4 之前和之后，静脉内施用L-NMMA（10mg/kg）或L-NAME（10mg/kg）显着增加（即逆转）MgSO 4 降低的血压，并且静脉内注射L-精氨酸部分恢复了L-NMMA和L-NAME两者的升高的血压作用。我们的结果表明，1）小血管非常依赖于 Mg 2 1 扩张的 NO 释放，2）细胞外 Mg 2 1 诱导的内皮依赖性松弛是通过内皮衍生的松弛因子-NO 的释放介导的，并且需要 Ca 2 1 和鸟苷 3 8 ,5 8 -环单磷酸的形成。
Mg 2 1 -induced endothelium-dependent relaxation of blood vessels and blood pressure lowering: role of NO. Am. J. Physiol. Regulatory Integrative Comp. Physiol. 278: R628–R639, 2000.—In vitro extracellular Mg 2 1 concentration ([Mg 2 1 ] 0 ) produces endothe-lium-dependent and endothelium-independent relaxations in rat aorta in a concentration-dependent manner. These relaxant effects of Mg 2 1 on intact rat aortic rings, but not denuded rat aortic rings, were suppressed by either N G -monomethyl- L arginine ( L -NMMA), N v -nitro- L -argininemethylester( L -NAME), or methylene blue. The inhibitory effects of L -NMMA and L -NAME could be reversed partly by L -arginine. [Mg 2 1 ] 0 induced dilatation in vivo in rat mesenteric arterioles and venules was almost completely inhibited by N G -nitro- L arginine and L -NMMA. Removal of extracellular Ca 2 1 concentration ([Ca 2 1 ] 0 ) or buffering intracellular Ca 2 1 concentration in endothelial cells, with 10 µM 1,2-bis(2-aminophenoxy)- ethane- N , N , N 8 , N 8 -tetraacetic acid-AM, markedly attenuated the relaxant effects of Mg 2 1 . Mg 2 1 produced nitric oxide (NO) release from the intact aortic rings in a concentration- dependent manner. Removal of [Ca 2 1 ] 0 diminished the increased NO release induced by elevated levels of [Mg 2 1 ] 0 . In vivo infusion of increasing doses (1–30 µM/min) of MgSO 4 , directly into the femoral veins of anesthetized rats, elicited significant concentration-dependent sustained increases in serum total Mg and concomitant decreases in arterial blood pressure. Before and after employment of various doses of MgSO 4 , intravenous administration of either L -NMMA (10 mg/kg) or L -NAME (10 mg/kg) increased (i.e., reversed) the MgSO 4 -lowered blood pressure markedly, and intravenous injection of L -arginine restored partially the increased blood pressure effects of both L -NMMA and L -NAME. Our results suggest that 1 ) small blood vessels are very dependent on NO release for Mg 2 1 dilatations and 2 ) the endothelium-depen-dent relaxation induced by extracellular Mg 2 1 is mediated by release of endothelium-derived relaxing factor-NO from the endothelium, and requires Ca 2 1 and formation of guanosine 3 8 ,5 8 -cyclic monophosphate.