Endogenous hydrogen sulfide regulation of myocardial injury induced by isoproterenol

Geng, Bin; Chang, Lin; Pan, Chun‐Shui; Qi, Yongcheng; Zhao, Jing; Pang, Yilin; Du, Junbao; Tang, Chaoshu

doi:10.1016/j.bbrc.2004.04.094

Cited by 368 publications

(266 citation statements)

References 36 publications

Supporting

Mentioning

243

Contrasting

Unclassified

Order By: Relevance

“…H 2 S plays an important role in the regulation of heart function. Together with other groups, we have found that both endogenous and exogenous H 2 S protect the heart from isoproterenol-induced myocardial injury by directly scavenging oxygen free radicals (Geng et al, 2004a) and inhibiting the adenylyl cyclase/ cAMP pathway or L-type calcium channel (Yong et al, 2008b). Moreover, researchers have found that preconditioning and postconditioning with H 2 S produced cardioprotective effects against ischemic injury via the regulation of protein kinase C, K ATP channels, cyclooxygenase-2, NO, p42/44-mitogen-activated protein kinase, phosphoinositol-3-kinase (PI3K)/Akt, and GSK3␤ pathways Yong et al, 2008a;Yao et al, 2010).…”

Section: Introductionsupporting

confidence: 56%

Hydrogen Sulfide Regulates Na⁺/H⁺ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways

Liu²,

Neo³

et al. 2011

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Intracellular pH (pH i ) is an important endogenous modulator of cardiac function. Inhibition of Naϩ /H ϩ exchanger-1 (NHE-1) protects the heart by preventing Ca 2ϩ overload during ischemia/reperfusion. Hydrogen sulfide (H 2 S) has been reported to produce cardioprotection. The present study was designed to investigate the pH regulatory effect of H 2 S in rat cardiac myocytes and evaluate its contribution to cardioprotection. It was found that sodium hydrosulfide (NaHS), at a concentration range of 10 to 1000 M, produced sustained decreases in pH i in the rat myocytes in a concentration-dependent manner. NaHS also abolished the intracellular alkalinization caused by trans-(Ϯ) -3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]benzeneacetamide methane-sulfonate hydrate (U50,488H), which activates NHEs. Moreover, when measured with an NHCl 4 prepulse method, NaHS was found to significantly suppress NHE-1 activity. Both NaHS and cariporide or [5-(2-methyl-5-fluorophenyl)furan-2-ylcarbonyl]guanidine (KR-32568), two NHE inhibitors, protected the myocytes against ischemia/reperfusion injury. However, coadministration of NaHS with KR-32568 did not produce any synergistic effect. Functional study showed that perfusion with NaHS significantly improved postischemic contractile function in isolated rat hearts subjected to ischemia/reperfusion. Blockade of phosphoinositide 3-kinase (PI3K) with 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002), Akt with Akt VIII, or protein kinase G (PKG) with (9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg: 3Ј,2Ј,1Ј-kl]pyrrolo[3,4-i][1,6]]enzodiazocine-10-carboxylic acid, methyl ester (KT5823) significantly attenuated NaHS-suppressed NHE-1 activity and/or NaHS-induced cardioprotection. Although KT5823 failed to affect NaHS-induced Akt phosphorylation, Akt inhibitor did attenuate NaHS-stimulated PKG activity. In conclusion, this work demonstrated for the first time that H 2 S produced cardioprotection via the suppression of NHE-1 activity involving a PI3K/Akt/PKG-dependent mechanism.

show abstract

Section: Introductionsupporting

confidence: 56%

Hydrogen Sulfide Regulates Na⁺/H⁺ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways

Liu²,

Neo³

et al. 2011

J Pharmacol Exp Ther

View full text Add to dashboard Cite

show abstract

“…So we tested the protein and mRNA expression of SUR2B and Kir6.1 in aortic and pulmonary arteries to investigate the possible mechanisms responsible for the regulation of vasorelaxation by H 2 S. H 2 S deficiency has been observed in animal models of systemic and pulmonary hypertension [16][17][18] . It also plays important roles in the pathogenesis of cardiovascular diseases [16][17][18][19][20][21][22][23][24] . The main mechanism for the cardiovascular actions of H 2 S was considered to be the activation of K ATP channels, because H 2 S increased whole-cell K ATP channel currents in rat aortic vascular smooth muscle cells [15] .…”

Section: Wwwchinapharcom Sun Y Et Almentioning

confidence: 99%

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

et al. 2011

View full text Add to dashboard Cite

Aim:To compare the vasorelaxing effects of hydrogen sulfide (H 2 S) on isolated aortic and pulmonary artery rings and to determine their action mechanisms. Methods: H 2 S-induced vasorelaxation of isolated rat aortic versus pulmonary artery rings under 95% O 2 and 5% CO 2 was analyzed. The expression of cystathinonine gamma-lyase (CSE), cystathionine beta synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3MST), SUR2B and Kir6.1 was examined. Results: NaHS caused vasorelaxation of rat aortic and pulmonary artery rings in a dose-dependent manner. NaHS dilated aortic rings to a greater extent (16.4%, 38.4%, 64.1%, 84.3%, and 95.9% at concentrations of 50, 100, 200, 500, and 1000 μmol/L, respectively) than pulmonary artery rings (10.1%, 22.2%, 50.6%, 73.6%, and 84.6% at concentrations of 50, 100, 200, 500 and 1000 μmol/L, respec tively). The EC 50 of the vasorelaxant effect for aortic rings was 152.17 μmol/L, whereas the EC 50 for pulmonary artery rings was 233.65 μmol/L. The vasorelaxing effect of H 2 S was markedly blocked b y cellular and mitochondrial membrane K ATP channel blockers in aortic rings (P<0.01). In contrast, only the cellular membrane K ATP channel blocker inhibited H 2 S-induced vasorelaxation in pulmonary artery rings. SUR2B mRNA and protein expression was higher in aortic rings than in pulmonary artery rings. Cystathinonine gamma-lyase (CSE) but not cystathionine beta synthase (CBS) expression in aortic rings was higher than in pulmonary artery rings. 3-Mercapto pyruvate sulfurtransferase (3MST) mRNA was lower in aortic rings than in pulmonary artery rings. Conclusion: The vasorelaxing effect of H 2 S on isolated aortic rings was more pronounced than the effect on pulmonary artery rings at specific concentrations, which might be associated with increased expression of the K ATP channel subunit SUR2B.

show abstract

“…Interestingly, NO and H 2 S can interact, and therefore changes in one system could impact the other (Hosoki et al 1997;Wang et al 2008). Additionally, H 2 S may also react with, and be quenched by, increased superoxide (Geng et al 2004a) as well as increased peroxynitrite produced from the reaction of NO with superoxide (Whiteman et al 2004). CR has been proposed to reduce age-related endothelial dysfunction by reducing the increase in superoxide production associated with aging, thereby maintaining a more youthful state (Barja 2002;Castello et al 2005;Gredilla et al 2004;Gredilla et al 2001;Taddei et al 2006).…”

Section: Cse and Cbs Protein Expressionmentioning

confidence: 99%

The hydrogen sulfide signaling system: changes during aging and the benefits of caloric restriction

Predmore

Alendy

Ahmed

et al. 2010

AGE

View full text Add to dashboard Cite

Hydrogen sulfide gas (H 2 S) is a putative signaling molecule that causes diverse effects in mammalian tissues including relaxation of blood vessels and regulation of perfusion in the liver, but the effects of aging on H 2 S signaling are unknown. Aging has negative impacts on the cardiovascular system. However, the liver is more resilient with age. Caloric restriction (CR) attenuates affects of age in many tissues. We hypothesized that the H 2 S signaling system is negatively affected by age in the vasculature but not in the liver, which is typically more resilient to age, and that a CR diet minimizes the age affect in the vasculature. To investigate this, we determined protein and mRNA expression of the H 2 S-producing enzymes cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS), H 2 S production rates in the aorta and liver, and the contractile response of aortic rings to exogenous H 2 S. Tissue was collected from Fisher 344×Brown Norway rats from 8-38 months of age, which had been maintained on an ad libitum (AL) or CR diet. The results demonstrate that age and diet have differential effects on the H 2 S signaling system in aorta and liver. The aorta showed a sizeable effect of both age and diet, whereas the liver only showed a sizeable effect of diet. Aortic rings showed increased contractile sensitivity to H 2 S and increased protein expression of CSE and CBS with age, consistent with a decrease in H 2 S concentration with age. CR appears to benefit CSE and CBS protein in both aorta and liver, potentially by reducing oxidative stress and ameliorating the negative effect of age on H 2 S concentration. Therefore, CR may help maintain the H 2 S signaling system during aging.

show abstract

Endogenous hydrogen sulfide regulation of myocardial injury induced by isoproterenol

Cited by 368 publications

References 36 publications

Hydrogen Sulfide Regulates Na⁺/H⁺ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways

Hydrogen Sulfide Regulates Na⁺/H⁺ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

The hydrogen sulfide signaling system: changes during aging and the benefits of caloric restriction

Contact Info

Product

Resources

About

Endogenous hydrogen sulfide regulation of myocardial injury induced by isoproterenol

Cited by 368 publications

References 36 publications

Hydrogen Sulfide Regulates Na+/H+ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways

Hydrogen Sulfide Regulates Na+/H+ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

The hydrogen sulfide signaling system: changes during aging and the benefits of caloric restriction

Contact Info

Product

Resources

About

Hydrogen Sulfide Regulates Na⁺/H⁺ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways

Hydrogen Sulfide Regulates Na⁺/H⁺ Exchanger Activity via Stimulation of Phosphoinositide 3-Kinase/Akt and Protein Kinase G Pathways