Interaction of Methylglyoxal and Hydrogen Sulfide in Rat Vascular Smooth Muscle Cells

2010 ◽  
Vol 12 (9) ◽  
pp. 1093-1100 ◽  
Author(s):  
Tuanjie Chang ◽  
Ashley Untereiner ◽  
Jianghai Liu ◽  
Lingyun Wu
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

Vasoconstrictive effect of hydrogen sulfide involves downregulation of cAMP in vascular smooth muscle cells

2008 ◽  
Vol 295 (5) ◽  
pp. C1261-C1270 ◽  
Author(s):  
Jia Jia Lim ◽  
Yi-Hong Liu ◽  
Ester Sandar Win Khin ◽  
Jin-Song Bian
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nitric Oxide Synthase Inhibitor ◽  
Vasorelaxant Effect ◽  
Synthase Inhibitor ◽  
Oxide Synthase

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.

scholarly journals Hydrogen sulfide inhibits the calcification and osteoblastic differentiation of vascular smooth muscle cells

2011 ◽  
Vol 80 (7) ◽  
pp. 731-739 ◽  
Author(s):  
Erzsébet Zavaczki ◽  
Viktória Jeney ◽  
Anupam Agarwal ◽  
Abolfazl Zarjou ◽  
Melinda Oros ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Osteoblastic Differentiation

Hydrogen sulfide-induced relaxation of resistance mesenteric artery beds of rats

2004 ◽  
Vol 287 (5) ◽  
pp. H2316-H2323 ◽  
Author(s):  
Youqin Cheng ◽  
Joseph Fomusi Ndisang ◽  
Guanghua Tang ◽  
Kun Cao ◽  
Rui Wang
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Vascular Effects ◽  
Rat Mesenteric Artery

Hydrogen sulfide (H2S) has been shown recently to function as an important gasotransmitter. The present study investigated the vascular effects of H2S, both exogenously applied and endogenously generated, on resistance mesenteric arteries of rats and the underlying mechanisms. Both H2S and NaHS evoked concentration-dependent relaxation of in vitro perfused rat mesenteric artery beds (MAB). The sensitivity of MAB to H2S (EC50, 25.2 ± 3.6 μM) was about fivefold higher than that of rat aortic tissues. Removal of endothelium or coapplication of charybdotoxin and apamin to endothelium-intact MAB significantly reduced the vasorelaxation effects of H2S. The H2S-induced relaxation of MAB was partially mediated by ATP-sensitive K+ (KATP) channel activity in vascular smooth muscle cells. Pinacidil (EC50, 1.7 ± 0.1 μM, n = 6) mimicked, but glibenclamide (10 μM, n = 6) suppressed, the vasorelaxant effect of H2S. KATP channel currents in isolated mesenteric artery smooth muscle cells were significantly augmented by H2S. l-Cysteine, a substrate of cystathionine-γ-lyase (CSE), at 1 mM increased endogenous H2S production by sixfold in rat mesenteric artery tissues and decreased contractility of MAB. dl-Propargylglycine (a blocker of CSE) at 10 μM abolished l-cysteine-dependent increase in H2S production and relaxation of MAB. Our results demonstrated a tissue-specific relaxant response of resistance arteries to H2S. The stimulation of KATP channels in vascular smooth muscle cells and charybdotoxin/apamin-sensitive K+ channels in vascular endothelium by H2S represents important cellular mechanisms for H2S effect on MAB. Our study also demonstrated that endogenous CSE can generate sufficient H2S from exogenous l-cysteine to cause vasodilation. Future studies are merited to investigate direct contribution of endogenous H2S to regulation of vascular tone.

Exogenous Hydrogen Sulfide Inhibits Superoxide Formation, NOX-1 Expression and Rac1 Activity in Human Vascular Smooth Muscle Cells

2008 ◽  
Vol 45 (6) ◽  
pp. 521-528 ◽  
Author(s):  
Saima Muzaffar ◽  
Nilima Shukla ◽  
Mark Bond ◽  
Andrew C. Newby ◽  
Gianni D. Angelini ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Superoxide Formation
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