Hydrogen sulfide as a vasodilator

Bhatia, Madhav

doi:10.1080/15216540500217875

Cited by 134 publications

(83 citation statements)

References 23 publications

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“…Similar to NO and CO, H 2 S, as a gaseous signaling molecule, has a number of physiological and pathological roles, such as cardioprotection (15,31), vasodilatation (32)(33)(34) and dermal protection (13,35). The endogenous formation of H 2 S is attributed to enzymes, such as cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (MPST) (12,19).…”

Section: Discussionmentioning

confidence: 99%

H2S inhibition of chemical hypoxia-induced proliferation of HPASMCs is mediated by the upregulation of COX-2/PGI2

Liu

Cai

et al. 2013

International Journal of Molecular Medicine

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Abstract. The hypoxia-induced proliferation of pulmonary artery smooth muscle cells (PASMCs) is the main cause of pulmonary arterial hypertension (PAH), in which oxidative stress, cyclooxygenase (COX)-2 and hydrogen sulfide (H 2 S) all play an important role. In the present study, we aimed to examine the effects of H 2 S on the hypoxia-induced proliferation of human PASMCs (HPASMCs) and to elucidate the underlying mechanisms. The HPASMCs were treated with cobalt chloride (CoCl 2 ), a hypoxia-mimicking agent, to establish a cellular model of hypoxic PAH. Prior to treatment with CoCl 2 , the cells were pre-conditioned with sodium hydrosulfide (NaHS), a donor of H 2 S. Cell proliferation, reactive oxygen species (ROS) production, COX-2 expression, prostacyclin (also known as prostaglandin I2 or PGI 2 ) secretion and H 2 S levels were detected in the cells. The exposure of the HPASMCs to CoCl 2 markedly increased cell proliferation, accompanied by a decrease in COX-2 expression, PGI 2 secretion and H 2 S levels; however, the levels of ROS were not altered. Although the exogenous ROS donor, H 2 O 2 , triggered similar degrees of proliferation to CoCl 2 , the ROS scavenger, N-acetyl-L-cysteine (NAC), markedly abolished the H 2 O 2 -induced cell proliferation, as opposed to the CoCl 2 -induced proliferation. The CoCl 2 -induced proliferation of HPASMCs was suppressed by exogenously applied PGI 2 . The addition of H 2 S (NaHS) attenuated the CoCl 2 -induced cell proliferation through the increase in the intercellular content of H 2 S. Importantly, the exposure of the cells to H 2 S suppressed the CoCl 2 -induced downregulation in COX-2 expression and PGI 2 secretion from the HPASMCs. In conclusion, the results from the current study suggest that H 2 S inhibits hypoxia-induced cell proliferation through the upregulation of COX-2/PGI 2 , as opposed to ROS.

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Section: Discussionmentioning

confidence: 99%

H2S inhibition of chemical hypoxia-induced proliferation of HPASMCs is mediated by the upregulation of COX-2/PGI2

Liu

Cai

et al. 2013

International Journal of Molecular Medicine

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“…The expression of SUR2B protein and mRNA in aortic rings increased compared to pulmonary artery rings. H 2 S, a novel gaseous signaling molecule, has been considered to play an important role in the regulation of cardiovascular functions [6][7][8][9][10] . Endogenous cardiovascular H 2 S is mainly produced by CSE [8][9][10] .…”

Section: Discussionmentioning

confidence: 99%

“…H 2 S, a novel gaseous signaling molecule, has been considered to play an important role in the regulation of cardiovascular functions [6][7][8][9][10] . Endogenous cardiovascular H 2 S is mainly produced by CSE [8][9][10] . R ecent evidence from CSE knockout mice suggests that loss of CSE gene expression results in a decrease in H 2 S production and a subsequent rise in blood pressure [16] .…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2011

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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.

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“…In the mammalian brain, H 2 S enhances responses that are linked to activation of NMDA receptors (1) while impeding the release of corticotrophin releasing factor from the hypothalamus (6,25). In the mammalian cardiovascular system, H 2 S has been portrayed almost exclusively as a vasodilator resulting from the relaxation of vascular smooth muscle (4,14,16,30,41,43,44). The principle mechanism underlying H 2 S-mediated relaxation of vascular smooth muscle is the activation of K ATP channels leading to cell membrane hyperpolarization (49).…”

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confidence: 99%

Hydrogen sulfide stimulates catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

Perry

McNeill²,

Elia³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Perry SF, McNeill B, Elia E, Nagpal A, Vulesevic B. Hydrogen sulfide stimulates catecholamine secretion in rainbow trout (Oncorhynchus mykiss). Am J Physiol Regul Integr Comp Physiol 296: R133-R140, 2009. First published November 5, 2008 doi:10.1152/ajpregu.00185.2008.-We tested the hypothesis that endogenously produced hydrogen sulfide (H 2S) can potentially contribute to the adrenergic stress response in rainbow trout by initiating catecholamine secretion from chromaffin cells. During acute hypoxia (water PO 2 ϭ 35 mmHg), plasma H2S levels were significantly elevated concurrently with a rise in circulating catecholamine concentrations. Tissues enriched with chromaffin cells (posterior cardinal vein and anterior kidney) produced H2S in vitro when incubated with L-cysteine. In both tissues, the production of H2S was eliminated by adding the cystathionine ␤-synthase inhibitor, aminooxyacetate. Cystathionine ␤-synthase and cystathionine ␥-lyase were cloned and sequenced and the results of real-time PCR demonstrated that with the exception of white muscle, mRNA for both enzymes was broadly distributed within the tissues that were examined. Electrical field stimulation of an in situ saline-perfused posterior cardinal vein preparation caused the appearance of H 2S and catecholamines in the outflowing perfusate. Perfusion with the cholinergic receptor agonist carbachol (1 ϫ 10 Ϫ6 M) or depolarizing levels of KCl (1 ϫ 10 Ϫ2 M) caused secretion of catecholamines without altering H 2S output, suggesting that neuronal excitation is required for H 2S release. Addition of H 2S (at concentrations exceeding 5 ϫ 10 Ϫ7 M) to the perfusion fluid resulted in a marked stimulation of catecholamine secretion that was not observed when Ca 2ϩ -free perfusate was used. These data, together with the finding that H 2S-induced catecholamine secretion was unaltered by the nicotinic receptor blocker hexamethonium, suggest that H 2S is able to directly elicit catecholamine secretion via membrane depolarization followed by Ca

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Hydrogen sulfide as a vasodilator

Cited by 134 publications

References 23 publications

H2S inhibition of chemical hypoxia-induced proliferation of HPASMCs is mediated by the upregulation of COX-2/PGI2

H2S inhibition of chemical hypoxia-induced proliferation of HPASMCs is mediated by the upregulation of COX-2/PGI2

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

Hydrogen sulfide stimulates catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

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