Back to Search
Start Over
P83: Hydrogen sulfide cytoprotective signaling is nitric oxide dependent.
- Source :
-
Nitric Oxide . May2014 Supplement, Vol. 39 Issue s1, pS40-S41. 0p. - Publication Year :
- 2014
-
Abstract
- Introduction: Consensus has formed that hydrogen sulfide (H2S) has robust cytoprotective actions in multiple organ systems. The pro-survival actions and biological profiles of H2S are remarkably similar to those of nitric oxide (NO). Although there is recent evidence of cross-talk between H2S and NO, these molecules are thought to modulate independent signaling pathways. Methods/Results: Mice devoid of the key H2S producing enzyme, cystathionine gamma-lyase (CSE KO), exhibited impaired endothelial nitric oxide synthase (eNOS) function and diminished circulating nitrite (0.41 uM vs 0.73μM, p <0.05) nitrosylated protein (3.37nM vs 15.03nM, p <0.05), and cyclic GMP (9.3 vs 28.05pmol/ml, p <0.01) levels compared to wild-type (WT) mice. Further studies revealed that H2S therapy in CSE KO mice restored eNOS function and NO levels. eNOS KO mice and mice with phospho-dead eNOS (S1179A) were subjected to 45min of ischemia, followed by 24h of reperfusion. The H2S donor, Na2S (100μg/kg), or vehicle (0.9% NaCl) was administered 5min before reperfusion. There was no significant change in myocardial infarction in the H2S-treated group compared to the vehicle-treated group. Conclusion: These findings reveal that H2S modulates eNOS activity and nitric oxide signaling. Moreover, the inability of H2S therapy to protect eNOS dysfunctional mice against myocardial ischemia/reperfusion injury indicates that the cardioprotective actions of H2S are dependent on eNOS function and NO signaling. [Copyright &y& Elsevier]
Details
- Language :
- English
- ISSN :
- 10898603
- Volume :
- 39
- Issue :
- s1
- Database :
- Academic Search Index
- Journal :
- Nitric Oxide
- Publication Type :
- Academic Journal
- Accession number :
- 96104064
- Full Text :
- https://doi.org/10.1016/j.niox.2014.03.133