The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Hydrogen Sulfide as Endothelium-Derived Hyperpolarizing Factor Sulfhydrates Potassium Channels
Open accessAbstract
Rationale: Nitric oxide, the classic endothelium-derived relaxing factor (EDRF), acts through cyclic GMP and calcium without notably affecting membrane potential. A major component of EDRF activity derives from hyperpolarization and is termed endothelium-derived hyperpolarizing factor (EDHF). Hydrogen sulfide (H 2 S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine γ-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. Objective: The purpose of this study was to determine if H 2 S is a major physiological EDHF. Methods and Results: We now show that H 2 S is a major EDHF because in blood vessels of CSE-deleted mice, hyperpolarization is virtually abolished. H 2 S acts by covalently modifying (sulfhydrating) the ATP-sensitive potassium channel, as mutating the site of sulfhydration prevents H 2 S-elicited hyperpolarization. The endothelial intermediate conductance (IK Ca ) and small conductance (SK Ca ) potassium channels mediate in part the effects of H 2 S, as selective IK Ca and SK Ca channel inhibitors, charybdotoxin and apamin, inhibit glibenclamide-insensitive, H 2 S-induced vasorelaxation. Conclusions: H 2 S is a major EDHF that causes vascular endothelial and smooth muscle cell hyperpolarization and vasorelaxation by activating the ATP-sensitive, intermediate conductance and small conductance potassium channels through cysteine S -sulfhydration. Because EDHF activity is a principal determinant of vasorelaxation in numerous vascular beds, drugs influencing H 2 S biosynthesis offer therapeutic potential.
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Cites
H 2 S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase
Yang, G., Wu, L., Jiang, B., Yang, W., Qi, J., Cao, K., Meng, Q., Mustafa, A. K., Mu, W., Zhang, S., et al. (2008) · Science · doi:10.1126/science.1162667 · Cited by 2,310
Self-citationProtein S-nitrosylation: Purview and parameters
Hess, D. T., Matsumoto, A., Kim, S.-O., Marshall, H. E., & Stamler, J. S. (2005) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1569 · Cited by 2,153
Hypertension in mice lacking the gene for endothelial nitric oxide synthase
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The discovery of nitric oxide and its role in vascular biology
Moncada, S., & Higgs, E. A. (2006) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0706458 · Cited by 863
Nitric Oxide and Cyclic GMP in Cell Signaling and Drug Development
Murad, F. (2006) · New England Journal of Medicine · doi:10.1056/nejmsa063904 · Cited by 420
Dorman, D. C. (2002) · Toxicological Sciences · doi:10.1093/toxsci/65.1.18 · Cited by 362
Impaired conduction of vasodilation along arterioles in connexin40-deficient mice
de Wit, C., Roos, F., Bolz, S.-S., Kirchhoff, S., Krüger, O., Willecke, K., & Pohl, U. (2000) · Circulation Research · doi:10.1161/01.res.86.6.649 · Cited by 338
Cited by
Coletta, C., Papapetropoulos, A., Erdelyi, K., Olah, G., Módis, K., Panopoulos, P., Asimakopoulou, A., Gerö, D., Sharina, I., Martin, E., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1202916109 · Cited by 677
Ethnobotany of medicinal plants among the communities of Alpine and Sub-alpine regions of Pakistan
Kayani, S., Ahmad, M., Sultana, S., Khan Shinwari, Z., Zafar, M., Yaseen, G., Hussain, M., & Bibi, T. (2015) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2015.02.004 · Cited by 391
Decreased Endogenous Production of Hydrogen Sulfide Accelerates Atherosclerosis
Mani, S., Li, H., Untereiner, A., Wu, L., Yang, G., Austin, R. C., Dickhout, J. G., Lhoták, Š., Meng, Q. H., & Wang, R. (2013) · Circulation · doi:10.1161/circulationaha.113.002208 · Cited by 377
Self-citationFilipovic, M. R., Miljkovic, J. L., Nauser, T., Royzen, M., Klos, K., Shubina, T., Koppenol, W. H., Lippard, S. J., & Ivanović-Burmazović, I. (2012) · Journal of the American Chemical Society · doi:10.1021/ja3009693 · Cited by 336
H2S and its role in redox signaling
Kabil, O., Motl, N., & Banerjee, R. (2014) · Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics · doi:10.1016/j.bbapap.2014.01.002 · Cited by 240
Metadata
- Authors
- Mustafa, A. K., Sikka, G., Gazi, S. K., Steppan, J., Jung, S. M., Bhunia, A. K., Barodka, V. M., Gazi, F. K., Barrow, R. K., Wang, R., Amzel, L. M., Berkowitz, D. E., & Snyder, S. H.
- Venue
- Circulation Research
- Published
- 2011-11-11
- Volume
- 109
- Issue
- 11
- Pages
- 1259-1268
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2131577505
- Cited by
- 622
- References
- 7
- FWCI
- 17.14
- Type
- journal article
- Language
- en
- Open access
- green
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- Mustafa, A. K., Sikka, G., Gazi, S. K., Steppan, J., Jung, S. M., Bhunia, A. K., Barodka, V. M., Gazi, F. K., Barrow, R. K., Wang, R., Amzel, L. M., Berkowitz, D. E., & Snyder, S. H. (2011). Hydrogen Sulfide as Endothelium-Derived Hyperpolarizing Factor Sulfhydrates Potassium Channels. Circulation Research. https://doi.org/10.1161/circresaha.111.240242
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