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Mineralocorticoid receptors contribute to ethanol-induced vascular hypercontractility through reactive oxygen species generation and up-regulation of cyclooxygenase 2
The effects on blood pressure produced byethanol consumption include both vasoconstriction and activation of the renin-angiotensin-aldosterone system (RAAS), although the detailed relationship between these processes is yet to be accomplished. Here, we sought to investigate the contribution of miner...
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| Published in: | European journal of pharmacology 2023-06, Vol.949, p.175723-175723, Article 175723 |
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| container_title | European journal of pharmacology |
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| creator | Dourado, Thales M.H. Assis, Victor O. Awata, Wanessa M.C. de Mello, Marcela M.B. Cárnio, Evelin C. Castro, Michele M. Tirapelli, Carlos R. |
| description | The effects on blood pressure produced byethanol consumption include both vasoconstriction and activation of the renin-angiotensin-aldosterone system (RAAS), although the detailed relationship between these processes is yet to be accomplished. Here, we sought to investigate the contribution of mineralocorticoid receptors (MR) to ethanol-induced hypertension and vascular hypercontractility. We analyzed blood pressure and vascular function of male Wistar Hannover rats treated with ethanol for five weeks. The contribution of the MR pathway to the cardiovascular effects of ethanol was evaluated with potassium canrenoate, a MR antagonist (MRA). Blockade of MR prevented ethanol-induced hypertension and hypercontractility of endothelium-intact and -denuded aortic rings. Ethanol up-regulated cyclooxygenase (COX)2 and augmented vascular levels of both reactive oxygen species (ROS) and thromboxane (TX)B2, a stable metabolite of TXA2. These responses were abrogated by MR blockade. Hyperreactivity to phenylephrine induced by ethanol consumption was reversed by tiron [a scavenger of superoxide (O2∙–)], SC236 (a selective COX2 inhibitor) or SQ29548 (an antagonist of TP receptors). Treatment with the antioxidant apocynin prevented the vascular hypercontractility, as well as the increases in COX2 expression and TXA2 production induced by ethanol consumption. Our study has identified novel mechanisms through which ethanol consumption promotes its deleterious effects in the cardiovascular system. We provided evidence for a role of MR in the vascular hypercontractility and hypertension associated with ethanol consumption. The MR pathway triggers vascular hypercontractility through ROS generation, up-regulation of COX2 and overproduction of TXA2, which will ultimately induce vascular contraction.
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| doi_str_mv | 10.1016/j.ejphar.2023.175723 |
| format | article |
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[Display omitted]</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2023.175723</identifier><identifier>PMID: 37059378</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Cyclooxygenase 2 ; Cyclooxygenase 2 - metabolism ; Endothelium, Vascular ; Ethanol ; Ethanol - adverse effects ; Hypertension - chemically induced ; Hypertension - metabolism ; Male ; Mineralocorticoid receptors ; Rats ; Rats, Wistar ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptors, Mineralocorticoid - metabolism ; Thromboxane A2 ; Up-Regulation ; Vasoconstriction</subject><ispartof>European journal of pharmacology, 2023-06, Vol.949, p.175723-175723, Article 175723</ispartof><rights>2023 Elsevier B.V.</rights><rights>Copyright © 2023 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-f05852b7e692726cf9fe5cb4b0b74679d5d28eae46ceebaf69df5b4c8523a6c63</citedby><cites>FETCH-LOGICAL-c362t-f05852b7e692726cf9fe5cb4b0b74679d5d28eae46ceebaf69df5b4c8523a6c63</cites><orcidid>0000-0002-9779-733X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37059378$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dourado, Thales M.H.</creatorcontrib><creatorcontrib>Assis, Victor O.</creatorcontrib><creatorcontrib>Awata, Wanessa M.C.</creatorcontrib><creatorcontrib>de Mello, Marcela M.B.</creatorcontrib><creatorcontrib>Cárnio, Evelin C.</creatorcontrib><creatorcontrib>Castro, Michele M.</creatorcontrib><creatorcontrib>Tirapelli, Carlos R.</creatorcontrib><title>Mineralocorticoid receptors contribute to ethanol-induced vascular hypercontractility through reactive oxygen species generation and up-regulation of cyclooxygenase 2</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>The effects on blood pressure produced byethanol consumption include both vasoconstriction and activation of the renin-angiotensin-aldosterone system (RAAS), although the detailed relationship between these processes is yet to be accomplished. Here, we sought to investigate the contribution of mineralocorticoid receptors (MR) to ethanol-induced hypertension and vascular hypercontractility. We analyzed blood pressure and vascular function of male Wistar Hannover rats treated with ethanol for five weeks. The contribution of the MR pathway to the cardiovascular effects of ethanol was evaluated with potassium canrenoate, a MR antagonist (MRA). Blockade of MR prevented ethanol-induced hypertension and hypercontractility of endothelium-intact and -denuded aortic rings. Ethanol up-regulated cyclooxygenase (COX)2 and augmented vascular levels of both reactive oxygen species (ROS) and thromboxane (TX)B2, a stable metabolite of TXA2. These responses were abrogated by MR blockade. Hyperreactivity to phenylephrine induced by ethanol consumption was reversed by tiron [a scavenger of superoxide (O2∙–)], SC236 (a selective COX2 inhibitor) or SQ29548 (an antagonist of TP receptors). Treatment with the antioxidant apocynin prevented the vascular hypercontractility, as well as the increases in COX2 expression and TXA2 production induced by ethanol consumption. Our study has identified novel mechanisms through which ethanol consumption promotes its deleterious effects in the cardiovascular system. We provided evidence for a role of MR in the vascular hypercontractility and hypertension associated with ethanol consumption. The MR pathway triggers vascular hypercontractility through ROS generation, up-regulation of COX2 and overproduction of TXA2, which will ultimately induce vascular contraction.
[Display omitted]</description><subject>Animals</subject><subject>Cyclooxygenase 2</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Endothelium, Vascular</subject><subject>Ethanol</subject><subject>Ethanol - adverse effects</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - metabolism</subject><subject>Male</subject><subject>Mineralocorticoid receptors</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, Mineralocorticoid - metabolism</subject><subject>Thromboxane A2</subject><subject>Up-Regulation</subject><subject>Vasoconstriction</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kc2O1SAUx4nROHdG38AYlm56BdpC2ZiYyfiRjHGja0Lh9JabXqhAb6Yv5HPKnY4uXXFy8v8I54fQG0r2lFD-_riH4zzquGeE1XsqWsHqZ2hHOyErIih7jnaE0KZiUsordJ3SkRDSSta-RFe1KFMtuh36_c15iHoKJsTsTHAWRzAw5xATNsHn6PolA84BQx61D1PlvF0MWHzWySyTjnhcZ4iPWm2ym1xecR5jWA5jybqszoDDw3oAj9MMxkHCZS6t2QWPtbd4masIhxL2uAkDNquZwubRCTB7hV4Mekrw-um9QT8_3f24_VLdf__89fbjfWVqznI1kLZrWS-ASyYYN4McoDV905NeNFxI21rWgYaGG4BeD1zaoe0bU0y15obXN-jdljvH8GuBlNXJJQPTpD2EJSnWESo7InldpM0mNTGkFGFQc3QnHVdFiboQUke1EVIXQmojVGxvnxqW_gT2n-kvkiL4sAmg_PPsIKpUTubLxV0hk5UN7v8NfwDPxqqx</recordid><startdate>20230615</startdate><enddate>20230615</enddate><creator>Dourado, Thales M.H.</creator><creator>Assis, Victor O.</creator><creator>Awata, Wanessa M.C.</creator><creator>de Mello, Marcela M.B.</creator><creator>Cárnio, Evelin C.</creator><creator>Castro, Michele M.</creator><creator>Tirapelli, Carlos R.</creator><general>Elsevier B.V</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><orcidid>https://orcid.org/0000-0002-9779-733X</orcidid></search><sort><creationdate>20230615</creationdate><title>Mineralocorticoid receptors contribute to ethanol-induced vascular hypercontractility through reactive oxygen species generation and up-regulation of cyclooxygenase 2</title><author>Dourado, Thales M.H. ; Assis, Victor O. ; Awata, Wanessa M.C. ; de Mello, Marcela M.B. ; Cárnio, Evelin C. ; Castro, Michele M. ; Tirapelli, Carlos R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-f05852b7e692726cf9fe5cb4b0b74679d5d28eae46ceebaf69df5b4c8523a6c63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Cyclooxygenase 2</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Endothelium, Vascular</topic><topic>Ethanol</topic><topic>Ethanol - adverse effects</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - metabolism</topic><topic>Male</topic><topic>Mineralocorticoid receptors</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, Mineralocorticoid - metabolism</topic><topic>Thromboxane A2</topic><topic>Up-Regulation</topic><topic>Vasoconstriction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dourado, Thales M.H.</creatorcontrib><creatorcontrib>Assis, Victor O.</creatorcontrib><creatorcontrib>Awata, Wanessa M.C.</creatorcontrib><creatorcontrib>de Mello, Marcela M.B.</creatorcontrib><creatorcontrib>Cárnio, Evelin C.</creatorcontrib><creatorcontrib>Castro, Michele M.</creatorcontrib><creatorcontrib>Tirapelli, Carlos R.</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><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dourado, Thales M.H.</au><au>Assis, Victor O.</au><au>Awata, Wanessa M.C.</au><au>de Mello, Marcela M.B.</au><au>Cárnio, Evelin C.</au><au>Castro, Michele M.</au><au>Tirapelli, Carlos R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mineralocorticoid receptors contribute to ethanol-induced vascular hypercontractility through reactive oxygen species generation and up-regulation of cyclooxygenase 2</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2023-06-15</date><risdate>2023</risdate><volume>949</volume><spage>175723</spage><epage>175723</epage><pages>175723-175723</pages><artnum>175723</artnum><issn>0014-2999</issn><eissn>1879-0712</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The effects on blood pressure produced byethanol consumption include both vasoconstriction and activation of the renin-angiotensin-aldosterone system (RAAS), although the detailed relationship between these processes is yet to be accomplished. Here, we sought to investigate the contribution of mineralocorticoid receptors (MR) to ethanol-induced hypertension and vascular hypercontractility. We analyzed blood pressure and vascular function of male Wistar Hannover rats treated with ethanol for five weeks. The contribution of the MR pathway to the cardiovascular effects of ethanol was evaluated with potassium canrenoate, a MR antagonist (MRA). Blockade of MR prevented ethanol-induced hypertension and hypercontractility of endothelium-intact and -denuded aortic rings. Ethanol up-regulated cyclooxygenase (COX)2 and augmented vascular levels of both reactive oxygen species (ROS) and thromboxane (TX)B2, a stable metabolite of TXA2. These responses were abrogated by MR blockade. Hyperreactivity to phenylephrine induced by ethanol consumption was reversed by tiron [a scavenger of superoxide (O2∙–)], SC236 (a selective COX2 inhibitor) or SQ29548 (an antagonist of TP receptors). Treatment with the antioxidant apocynin prevented the vascular hypercontractility, as well as the increases in COX2 expression and TXA2 production induced by ethanol consumption. Our study has identified novel mechanisms through which ethanol consumption promotes its deleterious effects in the cardiovascular system. We provided evidence for a role of MR in the vascular hypercontractility and hypertension associated with ethanol consumption. The MR pathway triggers vascular hypercontractility through ROS generation, up-regulation of COX2 and overproduction of TXA2, which will ultimately induce vascular contraction.
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| ispartof | European journal of pharmacology, 2023-06, Vol.949, p.175723-175723, Article 175723 |
| issn | 0014-2999 1879-0712 |
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| source | ScienceDirect Freedom Collection |
| subjects | Animals Cyclooxygenase 2 Cyclooxygenase 2 - metabolism Endothelium, Vascular Ethanol Ethanol - adverse effects Hypertension - chemically induced Hypertension - metabolism Male Mineralocorticoid receptors Rats Rats, Wistar Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, Mineralocorticoid - metabolism Thromboxane A2 Up-Regulation Vasoconstriction |
| title | Mineralocorticoid receptors contribute to ethanol-induced vascular hypercontractility through reactive oxygen species generation and up-regulation of cyclooxygenase 2 |
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