Mechanism of vasorelaxation and role of endogenous hydrogen sulfide production in mouse aorta
Mechanism of vasorelaxation and role of endogenous hydrogen sulfide production in mouse aorta
复制标题
DOI：
10.1007/s00210-011-0608-z
复制
发表时间：
2011-04-01
影响因子：
3.6
通讯作者：
Hart, Joanne L.
中科院分区：
文献类型：
--
作者：
Al-Magableh, Mohammad R.;Hart, Joanne L.
本研究旨在阐明h2s诱导血管舒张的分子机制。通过小血管肌图测量小鼠主动脉环的等长张力，研究了H2S供体NaHS和H2S前体l -半胱氨酸对血管松弛的反应。用极谱传感器测定Krebs溶液中H2S浓度。用Western blot检测H2S表达，用光谱学方法检测CSE产生的H2S。在预收缩的小鼠主动脉中，NaHS （1 μ M-3 mM）可引起血管松弛95+/-7%，EC50为189+/-69 μ m，这种反应不受内皮细胞去除的影响。K+通道阻断剂（50 mM K+）和K- atp通道阻断剂格列本脲（10 μ M）单独(P
This study aimed to elucidate the molecular mechanism of H2S-induced vasorelaxation. Vasorelaxation responses to the H2S donor NaHS and the H2S precursor L-cysteine were examined by measuring isometric tone of mouse aortic rings in a small vessel myograph. H2S concentrations in Krebs' solution were determined with a polarographic sensor. H2S expression was examined by Western blot, and H2S production from CSE was assayed using a spectroscopic method. In pre-constricted mouse aorta, NaHS (1 mu M-3 mM) elicited vasorelaxation of 95+/-7%, EC50 189+/-69 mu M. This response was unaffected by removal of the endothelium. Maximum vasorelaxation was significantly attenuated by global blockade of K+ channels (50 mM K+) and the K-ATP channel blocker glibenclamide (10 mu M) alone (P