Role of S-Nitrosation of Cysteine Residues in Long-Lasting Inhibitory Effect of Nitric Oxide on Arterial Tone
S- Nitrosation of cysteine residues plays an important role in nitric oxide (NO) signaling and transport. The aim of the present study was to investigate the role of S- nitrosothiols as a storage form of NO, which may account for the long-lasting effects in the vasculature. Rat aorta exposed to S- n...
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| Veröffentlicht in: | Molecular pharmacology 2003-05, Vol.63 (5), p.1148-1158 |
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| creator | Alencar, Jacicarlos L Lobysheva, Irina Geffard, Michel Sarr, Mamadou Schott, Christa Schini-Kerth, Valérie B Nepveu, Françoise Stoclet, Jean-Claude Muller, Bernard |
| description | S- Nitrosation of cysteine residues plays an important role in nitric oxide (NO) signaling and transport. The aim of the present
study was to investigate the role of S- nitrosothiols as a storage form of NO, which may account for the long-lasting effects in the vasculature. Rat aorta exposed
to S- nitrosoglutathione (GSNO) displayed, even after washout of the drug, a persistent increase in cysteine-NO residues (detected
by immunostaining using an antiserum that selectively recognized S- nitrosoproteins) and in NO content (detected by NO spin-trapping), a persistent attenuation of the effect of vasoconstrictors,
and a relaxant response upon addition of low molecular weight (LMW) thiols. Rat mesenteric and porcine coronary artery exposed
in vitro to GSNO, as well as aorta and mesenteric arteries removed from rats treated in vivo with GSNO, displayed similar
modifications of contraction. In isolated aorta exposed to GSNO, the decrease of the contractile response and the relaxant
effect of LMW thiols were both blunted by NO scavengers (oxyhemoglobin or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide)
or by a cyclic GMP-dependent protein kinase inhibitor (Rp-8-bromoguanosine-3â²,5â²-cyclic monophosphorothioate). In these arteries,
mercuric chloride (which cleaves the cysteine-NO bond) exerted a transient relaxation, completely abolished the one of LMW
thiols, and blunted the increase in cysteine-NO residues and NO content. Together, these data support the idea that S- nitrosation of cysteine residues is involved in long-lasting effects of NO on arterial tone. They suggest that S- nitrosation of tissue thiols is a mechanism of formation of local NO stores from which biologically active NO can subsequently
be released. |
| doi_str_mv | 10.1124/mol.63.5.1148 |
| format | Article |
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study was to investigate the role of S- nitrosothiols as a storage form of NO, which may account for the long-lasting effects in the vasculature. Rat aorta exposed
to S- nitrosoglutathione (GSNO) displayed, even after washout of the drug, a persistent increase in cysteine-NO residues (detected
by immunostaining using an antiserum that selectively recognized S- nitrosoproteins) and in NO content (detected by NO spin-trapping), a persistent attenuation of the effect of vasoconstrictors,
and a relaxant response upon addition of low molecular weight (LMW) thiols. Rat mesenteric and porcine coronary artery exposed
in vitro to GSNO, as well as aorta and mesenteric arteries removed from rats treated in vivo with GSNO, displayed similar
modifications of contraction. In isolated aorta exposed to GSNO, the decrease of the contractile response and the relaxant
effect of LMW thiols were both blunted by NO scavengers (oxyhemoglobin or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide)
or by a cyclic GMP-dependent protein kinase inhibitor (Rp-8-bromoguanosine-3â²,5â²-cyclic monophosphorothioate). In these arteries,
mercuric chloride (which cleaves the cysteine-NO bond) exerted a transient relaxation, completely abolished the one of LMW
thiols, and blunted the increase in cysteine-NO residues and NO content. Together, these data support the idea that S- nitrosation of cysteine residues is involved in long-lasting effects of NO on arterial tone. They suggest that S- nitrosation of tissue thiols is a mechanism of formation of local NO stores from which biologically active NO can subsequently
be released.</description><identifier>ISSN: 0026-895X</identifier><identifier>EISSN: 1521-0111</identifier><identifier>DOI: 10.1124/mol.63.5.1148</identifier><identifier>PMID: 12695543</identifier><language>eng</language><publisher>United States: American Society for Pharmacology and Experimental Therapeutics</publisher><subject>Animals ; Arteries - drug effects ; Arteries - metabolism ; Arteries - physiology ; Biochemistry, Molecular Biology ; Biophysics ; Cysteine - metabolism ; Life Sciences ; Male ; Nitric Oxide - physiology ; Nitric Oxide Donors - pharmacology ; Nitrosation ; Rats ; Rats, Wistar ; S-Nitrosoglutathione - pharmacology ; Sulfhydryl Compounds - metabolism ; Toxicology ; Vasoconstriction - drug effects</subject><ispartof>Molecular pharmacology, 2003-05, Vol.63 (5), p.1148-1158</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-efdea135b5c07c42835c9e688edbb556acb5ea378cbe60055eaccaf26193dfd3</citedby><cites>FETCH-LOGICAL-c354t-efdea135b5c07c42835c9e688edbb556acb5ea378cbe60055eaccaf26193dfd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12695543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00336053$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Alencar, Jacicarlos L</creatorcontrib><creatorcontrib>Lobysheva, Irina</creatorcontrib><creatorcontrib>Geffard, Michel</creatorcontrib><creatorcontrib>Sarr, Mamadou</creatorcontrib><creatorcontrib>Schott, Christa</creatorcontrib><creatorcontrib>Schini-Kerth, Valérie B</creatorcontrib><creatorcontrib>Nepveu, Françoise</creatorcontrib><creatorcontrib>Stoclet, Jean-Claude</creatorcontrib><creatorcontrib>Muller, Bernard</creatorcontrib><title>Role of S-Nitrosation of Cysteine Residues in Long-Lasting Inhibitory Effect of Nitric Oxide on Arterial Tone</title><title>Molecular pharmacology</title><addtitle>Mol Pharmacol</addtitle><description>S- Nitrosation of cysteine residues plays an important role in nitric oxide (NO) signaling and transport. The aim of the present
study was to investigate the role of S- nitrosothiols as a storage form of NO, which may account for the long-lasting effects in the vasculature. Rat aorta exposed
to S- nitrosoglutathione (GSNO) displayed, even after washout of the drug, a persistent increase in cysteine-NO residues (detected
by immunostaining using an antiserum that selectively recognized S- nitrosoproteins) and in NO content (detected by NO spin-trapping), a persistent attenuation of the effect of vasoconstrictors,
and a relaxant response upon addition of low molecular weight (LMW) thiols. Rat mesenteric and porcine coronary artery exposed
in vitro to GSNO, as well as aorta and mesenteric arteries removed from rats treated in vivo with GSNO, displayed similar
modifications of contraction. In isolated aorta exposed to GSNO, the decrease of the contractile response and the relaxant
effect of LMW thiols were both blunted by NO scavengers (oxyhemoglobin or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide)
or by a cyclic GMP-dependent protein kinase inhibitor (Rp-8-bromoguanosine-3â²,5â²-cyclic monophosphorothioate). In these arteries,
mercuric chloride (which cleaves the cysteine-NO bond) exerted a transient relaxation, completely abolished the one of LMW
thiols, and blunted the increase in cysteine-NO residues and NO content. Together, these data support the idea that S- nitrosation of cysteine residues is involved in long-lasting effects of NO on arterial tone. They suggest that S- nitrosation of tissue thiols is a mechanism of formation of local NO stores from which biologically active NO can subsequently
be released.</description><subject>Animals</subject><subject>Arteries - drug effects</subject><subject>Arteries - metabolism</subject><subject>Arteries - physiology</subject><subject>Biochemistry, Molecular Biology</subject><subject>Biophysics</subject><subject>Cysteine - metabolism</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Nitrosation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>S-Nitrosoglutathione - pharmacology</subject><subject>Sulfhydryl Compounds - metabolism</subject><subject>Toxicology</subject><subject>Vasoconstriction - drug effects</subject><issn>0026-895X</issn><issn>1521-0111</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkUFP4zAQRi0EgsLuca8rn5D2kGLHsZscq4oFpAgktoe9WY4zabxK7K7tAv33OGoFnEYzen4jz4fQD0rmlObFzeiGuWBznrqiPEEzynOaEUrpKZoRkousrPjfC3QZwj9CaMFLco4uaC4qzgs2Q-OzGwC7Dv_JHk30LqhonJ0Gq32IYCzgZwim3UHAxuLa2U1WqxCN3eAH25vGROf3-LbrQMfp2WQxGj-9mTZ5LV76CN6oAa-dhW_orFNDgO_HeoXWv2_Xq_usfrp7WC3rTDNexAy6FhRlvOGaLHSRl4zrCkRZQts0nAulGw6KLUrdgCCEp0Zr1eWCVqztWnaFfh20vRrk1ptR-b10ysj7ZS2nGSGMCcLZC03s9YHdevc__TLK0QQNw6AsuF2QC0arvCJVArMDqNOVgofuw0yJnKKQKQopmORyiiLxP4_iXTNC-0kfb_-5uTeb_tV4kNte-VFpN7jN_ovpHaP-kqM</recordid><startdate>20030501</startdate><enddate>20030501</enddate><creator>Alencar, Jacicarlos L</creator><creator>Lobysheva, Irina</creator><creator>Geffard, Michel</creator><creator>Sarr, Mamadou</creator><creator>Schott, Christa</creator><creator>Schini-Kerth, Valérie B</creator><creator>Nepveu, Françoise</creator><creator>Stoclet, Jean-Claude</creator><creator>Muller, Bernard</creator><general>American Society for Pharmacology and Experimental Therapeutics</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope></search><sort><creationdate>20030501</creationdate><title>Role of S-Nitrosation of Cysteine Residues in Long-Lasting Inhibitory Effect of Nitric Oxide on Arterial Tone</title><author>Alencar, Jacicarlos L ; Lobysheva, Irina ; Geffard, Michel ; Sarr, Mamadou ; Schott, Christa ; Schini-Kerth, Valérie B ; Nepveu, Françoise ; Stoclet, Jean-Claude ; Muller, Bernard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-efdea135b5c07c42835c9e688edbb556acb5ea378cbe60055eaccaf26193dfd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Arteries - drug effects</topic><topic>Arteries - metabolism</topic><topic>Arteries - physiology</topic><topic>Biochemistry, Molecular Biology</topic><topic>Biophysics</topic><topic>Cysteine - metabolism</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitrosation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>S-Nitrosoglutathione - pharmacology</topic><topic>Sulfhydryl Compounds - metabolism</topic><topic>Toxicology</topic><topic>Vasoconstriction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alencar, Jacicarlos L</creatorcontrib><creatorcontrib>Lobysheva, Irina</creatorcontrib><creatorcontrib>Geffard, Michel</creatorcontrib><creatorcontrib>Sarr, Mamadou</creatorcontrib><creatorcontrib>Schott, Christa</creatorcontrib><creatorcontrib>Schini-Kerth, Valérie B</creatorcontrib><creatorcontrib>Nepveu, Françoise</creatorcontrib><creatorcontrib>Stoclet, Jean-Claude</creatorcontrib><creatorcontrib>Muller, Bernard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Molecular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alencar, Jacicarlos L</au><au>Lobysheva, Irina</au><au>Geffard, Michel</au><au>Sarr, Mamadou</au><au>Schott, Christa</au><au>Schini-Kerth, Valérie B</au><au>Nepveu, Françoise</au><au>Stoclet, Jean-Claude</au><au>Muller, Bernard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of S-Nitrosation of Cysteine Residues in Long-Lasting Inhibitory Effect of Nitric Oxide on Arterial Tone</atitle><jtitle>Molecular pharmacology</jtitle><addtitle>Mol Pharmacol</addtitle><date>2003-05-01</date><risdate>2003</risdate><volume>63</volume><issue>5</issue><spage>1148</spage><epage>1158</epage><pages>1148-1158</pages><issn>0026-895X</issn><eissn>1521-0111</eissn><abstract>S- Nitrosation of cysteine residues plays an important role in nitric oxide (NO) signaling and transport. The aim of the present
study was to investigate the role of S- nitrosothiols as a storage form of NO, which may account for the long-lasting effects in the vasculature. Rat aorta exposed
to S- nitrosoglutathione (GSNO) displayed, even after washout of the drug, a persistent increase in cysteine-NO residues (detected
by immunostaining using an antiserum that selectively recognized S- nitrosoproteins) and in NO content (detected by NO spin-trapping), a persistent attenuation of the effect of vasoconstrictors,
and a relaxant response upon addition of low molecular weight (LMW) thiols. Rat mesenteric and porcine coronary artery exposed
in vitro to GSNO, as well as aorta and mesenteric arteries removed from rats treated in vivo with GSNO, displayed similar
modifications of contraction. In isolated aorta exposed to GSNO, the decrease of the contractile response and the relaxant
effect of LMW thiols were both blunted by NO scavengers (oxyhemoglobin or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide)
or by a cyclic GMP-dependent protein kinase inhibitor (Rp-8-bromoguanosine-3â²,5â²-cyclic monophosphorothioate). In these arteries,
mercuric chloride (which cleaves the cysteine-NO bond) exerted a transient relaxation, completely abolished the one of LMW
thiols, and blunted the increase in cysteine-NO residues and NO content. Together, these data support the idea that S- nitrosation of cysteine residues is involved in long-lasting effects of NO on arterial tone. They suggest that S- nitrosation of tissue thiols is a mechanism of formation of local NO stores from which biologically active NO can subsequently
be released.</abstract><cop>United States</cop><pub>American Society for Pharmacology and Experimental Therapeutics</pub><pmid>12695543</pmid><doi>10.1124/mol.63.5.1148</doi><tpages>11</tpages></addata></record> |
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| subjects | Animals Arteries - drug effects Arteries - metabolism Arteries - physiology Biochemistry, Molecular Biology Biophysics Cysteine - metabolism Life Sciences Male Nitric Oxide - physiology Nitric Oxide Donors - pharmacology Nitrosation Rats Rats, Wistar S-Nitrosoglutathione - pharmacology Sulfhydryl Compounds - metabolism Toxicology Vasoconstriction - drug effects |
| title | Role of S-Nitrosation of Cysteine Residues in Long-Lasting Inhibitory Effect of Nitric Oxide on Arterial Tone |
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