Ahmed A H, Maulood I M
Bratisl Lek Listy. 2018;119(7):444-449. doi: 10.4149/BLL_2018_081.
The aim of this study was to evaluate the possible roles of endothelin-1 and angiotensin-II in urotensin-II vasoconstriction and in endothelial dysfunction induced by mercury.
Urotensin-II, the most potent vasoactive peptide, is entwined with the cardiovascular diseases and has been labelled as a new pathophysiological biomarker.
Rat aortic rings were pre-incubated with sb-710411, bq-123, and captopril. Doses of human urotensin-II with increased concentrations were applied in all groups in the presence or absence of mercury chloride. In another set of the experiment, aortic rings were treated with a single dose of mercury chloride in the presence of each of the above blockers.
Angiotensin-II and endothelin-1 mediated the vascular responses to the peptide urotensin-II under conditions of both intact endothelium and endothelial impairments induced by mercury. Urotensin-II, angiotensin-II and endothelin-1 significantly participated in vascular responses to mercury chloride.
The novel finding was that urotensin-II is potentiated under the condition of endothelial dysfunction. Endothelin-1 and angiotensin-II pathways could be heavily exploited in modulating endothelial dysfunction impacts and peptide vascular actions (Tab. 1, Fig. 4, Ref. 30).
本研究旨在评估内皮素 -1 和血管紧张素 -II 在尾加压素 -II 血管收缩以及汞诱导的内皮功能障碍中可能发挥的作用。
尾加压素 -II 是最有效的血管活性肽，与心血管疾病相关，已被标记为一种新的病理生理生物标志物。
大鼠主动脉环先用 sb -710411、bq -123 和卡托普利进行预孵育。在存在或不存在氯化汞的情况下，对所有组施加浓度递增的人尾加压素 -II 剂量。在另一组实验中，在上述每种阻滞剂存在的情况下，用单剂量氯化汞处理主动脉环。
在完整内皮和汞诱导的内皮损伤条件下，血管紧张素 -II 和内皮素 -1 介导了血管对尾加压素 -II 的反应。尾加压素 -II、血管紧张素 -II 和内皮素 -1 显著参与了对氯化汞的血管反应。
新发现是尾加压素 -II 在内皮功能障碍条件下增强。内皮素 -1 和血管紧张素 -II 途径在调节内皮功能障碍影响和肽的血管作用方面可得到大量应用（表 1，图 4，参考文献 30）。
