Thomas G, Hecker M, Ramwell P W
Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, D.C. 20007
Biochem Biophys Res Commun. 1989 Jan 16;158(1):177-80. doi: 10.1016/s0006-291x(89)80194-9.
Irrespective of their stereochemistry (D- or L-form), polycations such as poly-lysine, poly-arginine and poly-histidine elicited endothelium dependent relaxation of pre-contracted rat aortic rings in a dose-dependent manner (ED50 less than or equal to 10-7 M). In contrast, the basic amino acids arginine, glutamine, histidine and lysine caused only endothelium-potentiated relaxation at high concentrations (ED 50 greater than 10-3 M). Both heparin (1U/ml) and dextran sulphate (10 microgram/ml) abolished relaxation by the polycations but had no effect on the responses to the basic amino acids or acetylcholine. These results indicate that the vasodilatory property of the polycations is due to an electrostatic interaction with anionic domains on the endothelial surface, whereas the basic amino acids elicit a non-specific relaxation. Therefore, L-arginine per se cannot be the immediate precursor of nitric oxide, the proposed endothelium-derived relaxing factor.
无论其立体化学结构（D型或L型）如何，诸如聚赖氨酸、聚精氨酸和聚组氨酸等聚阳离子均能以剂量依赖的方式引起预收缩的大鼠主动脉环的内皮依赖性舒张（半数有效剂量小于或等于10-7M）。相比之下，碱性氨基酸精氨酸、谷氨酰胺、组氨酸和赖氨酸仅在高浓度时引起内皮增强的舒张（半数有效剂量大于10-3M）。肝素（1U/ml）和硫酸葡聚糖（10微克/ml）均可消除聚阳离子引起的舒张，但对碱性氨基酸或乙酰胆碱的反应无影响。这些结果表明，聚阳离子的血管舒张特性是由于与内皮表面阴离子结构域的静电相互作用，而碱性氨基酸引起的是非特异性舒张。因此，L-精氨酸本身不可能是一氧化氮（即所谓的内皮源性舒张因子）的直接前体。
