Glusa E
University of Jena, Medical School, Center for Vascular Biology and Medicine, Erfurt, Germany.
Thromb Haemost. 1994 Aug;72(2):318-21.
Desulfated hirugen (hirudin 54-65) at concentrations from 0.1 to 2 microM was found to relax PGF2 alpha-precontracted ring segments of porcine pulmonary arteries with intact endothelium. The relaxation was associated with a pronounced increase in cGMP in the vessels. This endothelium-dependent relaxant effect depended on the extracellular calcium ion concentration and was probably due to the release of endothelium-derived NO as indicated by its susceptibility to blockade of the NO synthesis by NG-nitro-L-arginine. In the presence of indomethacin (3 microM) the maximum hirugen effect was significantly diminished by about 25%. In contrast, neither the sulfated hirugen nor recombinant desulfato hirudin at equimolar concentrations exerted endothelium-dependent relaxation. Hence, the relaxant effect did not correspond to the anticoagulant activity. Desulfated hirugen can be assigned to the group of well-known peptides causing vasodilatation via an endothelium-dependent mechanism.
已发现浓度为0.1至2微摩尔的去硫酸化水蛭素（水蛭素54 - 65）可使具有完整内皮的猪肺动脉PGF2α预收缩环段舒张。这种舒张与血管中cGMP的显著增加有关。这种内皮依赖性舒张作用取决于细胞外钙离子浓度，并且可能是由于内皮源性一氧化氮（NO）的释放，这可由其对NG - 硝基 - L - 精氨酸抑制NO合成的敏感性表明。在吲哚美辛（3微摩尔）存在的情况下，水蛭素的最大作用显著降低约25%。相比之下，等摩尔浓度的硫酸化水蛭素和重组去硫酸化水蛭素均未产生内皮依赖性舒张作用。因此，舒张作用与抗凝活性不对应。去硫酸化水蛭素可归为通过内皮依赖性机制引起血管舒张的一类知名肽。
