Endothelium-dependent L-Arg- and L-NMMA-sensitive mechanisms regulate tone of brain microvessels.
Endothelium-dependent L-Arg- and L-NMMA-sensitive mechanisms regulate tone of brain microvessels.
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内皮依赖性 L-Arg 和 L-NMMA 敏感机制调节脑微血管的张力。
DOI：
10.1152/ajpheart.1990.259.5.h1396
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Nelson,GH
中科院分区：
文献类型：
--
作者：
Rosenblum,WI;Nishimura,H;Nelson,GH
通过电视显微镜观察小鼠脑表面的软脑膜小动脉，并用图像分裂技术进行测量。低至10（-5）M浓度的L-精氨酸（L-Arg）可使血管扩张，NG-单甲基-L-精氨酸（L-NMMA）则呈剂量依赖性地使血管收缩。内皮细胞损伤可使血管扩张和收缩消失。这种损伤是通过一种成熟的技术在短段内皮上产生的，该技术包括在血管内伊文思蓝染料存在的情况下将内皮暴露于氦氖激光。在对10（-5）M L-Arg有反应的小动脉中，同样在10（-5）M浓度下的其他5种L-氨基酸没有任何作用。这些数据提供了直接的证据，内皮依赖性的反应，L-Arg和L-NMMA在体内的脑血管系统的一个定义的部分。L-NMMA抑制L-Arg或乙酰胆碱的扩张。这些数据与体外研究和证明L-NMMA急性升高血压的研究数据一致。从所有这些早期的研究中，已经假设有一种持续作用的、内皮依赖性的、L-Arg依赖性的和L-NMMA可降解的机制倾向于舒张血管。该机制的介质被认为是乙酰胆碱的内皮依赖性舒张因子。我们的数据表明，这种机制是在体内的大脑的阻力血管。
Pial arterioles on the surface of the mouse brain were observed via television microscopy and measured with an image-splitting technique. The vessels were dilated by L-arginine (L-Arg) in concentrations as low as 10(-5) M and were constricted in dose-dependent manner by NG-monomethyl-L-arginine (L-NMMA). Both the dilation and the constriction were abolished by endothelial damage. This damage was produced over a short segment of endothelium by a well-established technique that involves exposing the endothelium to a helium-neon laser in the presence of intravascular Evans blue dye. In arterioles that were responsive to 10(-5) M L-Arg, five other L-amino acids, also at 10(-5) M, failed to have any effect. The data provide direct evidence for the endothelium-dependent nature of the responses to L-Arg and L-NMMA in vivo in a defined segment of the cerebral vasculature. L-NMMA inhibited dilation by either L-Arg or acetylcholine. The data are consistent with data from in vitro studies and from studies demonstrating that L-NMMA acutely raises blood pressure. From all these earlier studies it has been hypothesized that there is a continuously acting, endothelium-dependent, L-Arg-dependent, and L-NMMA-inhibitable mechanism tending to relax blood vessels. The mediator of this mechanism is thought to be the endothelium-dependent relaxing factor for acetylcholine. Our data suggest that this mechanism is acting in the resistance vessels of the brain in vivo.