Hydrogen sulfide inhibited L-type calcium channels (CaV1.2) via up-regulation of the channel sulfhydration in vascular smooth muscle cells

2019 ◽  
Vol 858 ◽  
pp. 172455 ◽  
Author(s):  
Li Dai ◽  
Yuanyuan Qian ◽  
Jun Zhou ◽  
Chao Zhu ◽  
Lai Jin ◽  
...  
2003 ◽  
Vol 44 (6) ◽  
pp. 963-978 ◽  
Author(s):  
Toshiaki Nakajima ◽  
Ji Ma ◽  
Haruko Iida ◽  
Kuniaki Iwasawa ◽  
Taisuke Jo ◽  
...  

2010 ◽  
Vol 12 (9) ◽  
pp. 1093-1100 ◽  
Author(s):  
Tuanjie Chang ◽  
Ashley Untereiner ◽  
Jianghai Liu ◽  
Lingyun Wu

2008 ◽  
Vol 295 (5) ◽  
pp. C1261-C1270 ◽  
Author(s):  
Jia Jia Lim ◽  
Yi-Hong Liu ◽  
Ester Sandar Win Khin ◽  
Jin-Song Bian

Hydrogen sulfide (H2S), a new endogenous mediator, produces both vasorelaxation and vasoconstriction. This study was designed to examine whether cAMP mediates the vasoconstrictive effect of H2S. We found that NaHS at a concentration range of 10–100 μM (yields ∼3–30 μM H2S) concentration-dependently reversed the vasodilation caused by isoprenaline and salbutamol, two β-adrenoceptor agonists, and forskolin, a selective adenylyl cyclase activator, in phenylephrine-precontracted rat aortic rings. Pretreatment with NaHS (10–100 μM) for 5 min also significantly attenuated the vasorelaxant effect of salbutamol and forskolin. More importantly, NaHS (5–100 μM) significantly reversed forskolin-induced cAMP accumulation in vascular smooth muscle cells. However, NaHS produced significant, but weaker, vasoconstriction in the presence of NG-nitro-l-arginine methyl ester (100 μM), a nitric oxide synthase inhibitor, or in endothelium-denuded aortic rings. Blockade of ATP-sensitive potassium channels with glibenclamide (10 μM) failed to attenuate the vasoconstriction induced by H2S. Taken together, we demonstrated for the first time that the vasoconstrictive effect of H2S involves the adenyly cyclase/cAMP pathway.


2011 ◽  
Vol 80 (7) ◽  
pp. 731-739 ◽  
Author(s):  
Erzsébet Zavaczki ◽  
Viktória Jeney ◽  
Anupam Agarwal ◽  
Abolfazl Zarjou ◽  
Melinda Oros ◽  
...  

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