Effects of Angiotensin-1 Converting Enzyme Inhibition on Oxidative Stress and Bradykinin Receptor Expression During Doxorubicin-induced Cardiomyopathy in Rats
To evaluate the mechanisms and the impact of the angiotensin-converting enzyme inhibitor perindopril (P) in a model of doxorubicin (D)-induced cardiotoxicity, male Wistar rats received D (1 mg/kg/d, IP for 10 days), P (2 mg/kg/d by gavage from day 1 to day 18), D (for 10 days) + P (for 18 days) or s...
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| Veröffentlicht in: | Journal of cardiovascular pharmacology 2008-09, Vol.52 (3), p.278-285 |
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| creator | Richard, Carole Lauzier, Benjamin Delemasure, Stéphanie Talbot, Sébastien Ghibu, Stéliana Collin, Bertrand Sénécal, Jacques Menetrier, Franck Vergely, Catherine Couture, Réjean Rochette, Luc |
| description | To evaluate the mechanisms and the impact of the angiotensin-converting enzyme inhibitor perindopril (P) in a model of doxorubicin (D)-induced cardiotoxicity, male Wistar rats received D (1 mg/kg/d, IP for 10 days), P (2 mg/kg/d by gavage from day 1 to day 18), D (for 10 days) + P (for 18 days) or saline. D decreased systolic blood pressure and body and heart weights. Left ventricular diastolic diameter was increased by D (P < 0.01), but it was not attenuated by P. D decreased plasma vitamin C (P < 0.05) and increased the ascorbyl radical/vitamin C ratio (P < 0.01). This ratio was attenuated by P. No difference was found among groups in cardiac troponin I, brain natriuretic peptide concentrations, and tissue oxidative stress (OS). Myocardial MCP-1 expression was higher in the D group. Cardiac kinin receptor (B1R and B2R) expression was not affected by D, yet binding sites for B2R and B1R were increased in D+P and P groups, respectively (P < 0.05). In conclusion, D induced cardiac functional alterations, inflammation and plasma OS whereas tissue OS, and cardiac kinin receptors expression were not modified. P did not improve cardiac performance, but it modulated kinin receptor expression and enhanced antioxidant defense. |
| doi_str_mv | 10.1097/FJC.0b013e3181865f28 |
| format | Article |
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D decreased systolic blood pressure and body and heart weights. Left ventricular diastolic diameter was increased by D (P < 0.01), but it was not attenuated by P. D decreased plasma vitamin C (P < 0.05) and increased the ascorbyl radical/vitamin C ratio (P < 0.01). This ratio was attenuated by P. No difference was found among groups in cardiac troponin I, brain natriuretic peptide concentrations, and tissue oxidative stress (OS). Myocardial MCP-1 expression was higher in the D group. Cardiac kinin receptor (B1R and B2R) expression was not affected by D, yet binding sites for B2R and B1R were increased in D+P and P groups, respectively (P < 0.05). In conclusion, D induced cardiac functional alterations, inflammation and plasma OS whereas tissue OS, and cardiac kinin receptors expression were not modified. P did not improve cardiac performance, but it modulated kinin receptor expression and enhanced antioxidant defense.</description><identifier>ISSN: 0160-2446</identifier><identifier>EISSN: 1533-4023</identifier><identifier>DOI: 10.1097/FJC.0b013e3181865f28</identifier><identifier>PMID: 18806609</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins, Inc</publisher><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Animals ; Antibiotics, Antineoplastic - toxicity ; Ascorbic Acid - blood ; Binding Sites ; Blood Pressure - drug effects ; Cardiology and cardiovascular system ; Cardiomyopathies - chemically induced ; Cardiomyopathies - drug therapy ; Chemokine CCL2 - metabolism ; Doxorubicin - toxicity ; Gene Expression Regulation - drug effects ; Human health and pathology ; Life Sciences ; Male ; Natriuretic Peptide, Brain - drug effects ; Natriuretic Peptide, Brain - metabolism ; Oxidative Stress - drug effects ; Perindopril - pharmacology ; Rats ; Rats, Wistar ; Receptor, Bradykinin B1 - drug effects ; Receptor, Bradykinin B1 - metabolism ; Receptor, Bradykinin B2 - drug effects ; Receptor, Bradykinin B2 - metabolism ; Troponin I - drug effects ; Troponin I - metabolism</subject><ispartof>Journal of cardiovascular pharmacology, 2008-09, Vol.52 (3), p.278-285</ispartof><rights>2008 Lippincott Williams & Wilkins, Inc.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4960-c388ed50499d37efaa2e59bff106a1fa1fffbf9ab8cc986c600b439bfe6b227d3</citedby><cites>FETCH-LOGICAL-c4960-c388ed50499d37efaa2e59bff106a1fa1fffbf9ab8cc986c600b439bfe6b227d3</cites><orcidid>0000-0002-1370-6155 ; 0000-0003-4009-776X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf><![CDATA[$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&PDF=y&D=ovft&AN=00005344-200809000-00010$$EPDF$$P50$$Gwolterskluwer$$H]]></linktopdf><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00005344-200809000-00010$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>230,315,781,785,886,4610,27929,27930,64671,65466</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18806609$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://u-bourgogne.hal.science/hal-03437191$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Richard, Carole</creatorcontrib><creatorcontrib>Lauzier, Benjamin</creatorcontrib><creatorcontrib>Delemasure, Stéphanie</creatorcontrib><creatorcontrib>Talbot, Sébastien</creatorcontrib><creatorcontrib>Ghibu, Stéliana</creatorcontrib><creatorcontrib>Collin, Bertrand</creatorcontrib><creatorcontrib>Sénécal, Jacques</creatorcontrib><creatorcontrib>Menetrier, Franck</creatorcontrib><creatorcontrib>Vergely, Catherine</creatorcontrib><creatorcontrib>Couture, Réjean</creatorcontrib><creatorcontrib>Rochette, Luc</creatorcontrib><title>Effects of Angiotensin-1 Converting Enzyme Inhibition on Oxidative Stress and Bradykinin Receptor Expression During Doxorubicin-induced Cardiomyopathy in Rats</title><title>Journal of cardiovascular pharmacology</title><addtitle>J Cardiovasc Pharmacol</addtitle><description>To evaluate the mechanisms and the impact of the angiotensin-converting enzyme inhibitor perindopril (P) in a model of doxorubicin (D)-induced cardiotoxicity, male Wistar rats received D (1 mg/kg/d, IP for 10 days), P (2 mg/kg/d by gavage from day 1 to day 18), D (for 10 days) + P (for 18 days) or saline. D decreased systolic blood pressure and body and heart weights. Left ventricular diastolic diameter was increased by D (P < 0.01), but it was not attenuated by P. D decreased plasma vitamin C (P < 0.05) and increased the ascorbyl radical/vitamin C ratio (P < 0.01). This ratio was attenuated by P. No difference was found among groups in cardiac troponin I, brain natriuretic peptide concentrations, and tissue oxidative stress (OS). Myocardial MCP-1 expression was higher in the D group. Cardiac kinin receptor (B1R and B2R) expression was not affected by D, yet binding sites for B2R and B1R were increased in D+P and P groups, respectively (P < 0.05). In conclusion, D induced cardiac functional alterations, inflammation and plasma OS whereas tissue OS, and cardiac kinin receptors expression were not modified. P did not improve cardiac performance, but it modulated kinin receptor expression and enhanced antioxidant defense.</description><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Antibiotics, Antineoplastic - toxicity</subject><subject>Ascorbic Acid - blood</subject><subject>Binding Sites</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiology and cardiovascular system</subject><subject>Cardiomyopathies - chemically induced</subject><subject>Cardiomyopathies - drug therapy</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Doxorubicin - toxicity</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Human health and pathology</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Natriuretic Peptide, Brain - drug effects</subject><subject>Natriuretic Peptide, Brain - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Perindopril - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Bradykinin B1 - drug effects</subject><subject>Receptor, Bradykinin B1 - metabolism</subject><subject>Receptor, Bradykinin B2 - drug effects</subject><subject>Receptor, Bradykinin B2 - metabolism</subject><subject>Troponin I - drug effects</subject><subject>Troponin I - metabolism</subject><issn>0160-2446</issn><issn>1533-4023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd1u3CAQha2qVbNN-wZVxW0vnAwGY3O53WyaVCtF6s-1hQ3ENF6wAG_WfZg-a7A2aqSiQWjgfAeNTpZ9xHCBgVeX1982F9ACJorgGtes1EX9KlvhkpCcQkFeZyvADPKCUnaWvQvhNwCmZcXeZme4roEx4Kvs71Zr1cWAnEZre29cVDYYm2O0cfagfDT2Hm3tn3mv0K3tTWuicRalujsaKaI5KPQjehUCElaiL17I-cFYY9F31akxOo-2x3F5X7CryS9-V-7o_NSaLn1krJw6JdFGeGncfnajiP2MFgMRw_vsjRZDUB-ez_Ps1_X25-Ym3919vd2sd3lHeZqxI3WtZAmUc0kqpYUoVMlbrTEwgXUqrVvNRVt3Ha9ZxwBaSpJAsbYoKknOs88n314MzejNXvi5ccI0N-tds9wBoaTCHB9w0tKTtvMuBK_0PwBDs0TTpGia_6NJ2KcTNk7tXskX6DmLF99HN0Tlw8MwPSrf9EoMsW8grZJQmhcANfDU5WljIE81x55M</recordid><startdate>200809</startdate><enddate>200809</enddate><creator>Richard, Carole</creator><creator>Lauzier, Benjamin</creator><creator>Delemasure, Stéphanie</creator><creator>Talbot, Sébastien</creator><creator>Ghibu, Stéliana</creator><creator>Collin, Bertrand</creator><creator>Sénécal, Jacques</creator><creator>Menetrier, Franck</creator><creator>Vergely, Catherine</creator><creator>Couture, Réjean</creator><creator>Rochette, Luc</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott, Williams & Wilkins</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>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0002-1370-6155</orcidid><orcidid>https://orcid.org/0000-0003-4009-776X</orcidid></search><sort><creationdate>200809</creationdate><title>Effects of Angiotensin-1 Converting Enzyme Inhibition on Oxidative Stress and Bradykinin Receptor Expression During Doxorubicin-induced Cardiomyopathy in Rats</title><author>Richard, Carole ; Lauzier, Benjamin ; Delemasure, Stéphanie ; Talbot, Sébastien ; Ghibu, Stéliana ; Collin, Bertrand ; Sénécal, Jacques ; Menetrier, Franck ; Vergely, Catherine ; Couture, Réjean ; Rochette, Luc</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4960-c388ed50499d37efaa2e59bff106a1fa1fffbf9ab8cc986c600b439bfe6b227d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Antibiotics, Antineoplastic - toxicity</topic><topic>Ascorbic Acid - blood</topic><topic>Binding Sites</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology and cardiovascular system</topic><topic>Cardiomyopathies - chemically induced</topic><topic>Cardiomyopathies - drug therapy</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Doxorubicin - toxicity</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Human health and pathology</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Natriuretic Peptide, Brain - drug effects</topic><topic>Natriuretic Peptide, Brain - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>Perindopril - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Bradykinin B1 - drug effects</topic><topic>Receptor, Bradykinin B1 - metabolism</topic><topic>Receptor, Bradykinin B2 - drug effects</topic><topic>Receptor, Bradykinin B2 - metabolism</topic><topic>Troponin I - drug effects</topic><topic>Troponin I - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Richard, Carole</creatorcontrib><creatorcontrib>Lauzier, Benjamin</creatorcontrib><creatorcontrib>Delemasure, Stéphanie</creatorcontrib><creatorcontrib>Talbot, Sébastien</creatorcontrib><creatorcontrib>Ghibu, Stéliana</creatorcontrib><creatorcontrib>Collin, Bertrand</creatorcontrib><creatorcontrib>Sénécal, Jacques</creatorcontrib><creatorcontrib>Menetrier, Franck</creatorcontrib><creatorcontrib>Vergely, Catherine</creatorcontrib><creatorcontrib>Couture, Réjean</creatorcontrib><creatorcontrib>Rochette, Luc</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Journal of cardiovascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Richard, Carole</au><au>Lauzier, Benjamin</au><au>Delemasure, Stéphanie</au><au>Talbot, Sébastien</au><au>Ghibu, Stéliana</au><au>Collin, Bertrand</au><au>Sénécal, Jacques</au><au>Menetrier, Franck</au><au>Vergely, Catherine</au><au>Couture, Réjean</au><au>Rochette, Luc</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Angiotensin-1 Converting Enzyme Inhibition on Oxidative Stress and Bradykinin Receptor Expression During Doxorubicin-induced Cardiomyopathy in Rats</atitle><jtitle>Journal of cardiovascular pharmacology</jtitle><addtitle>J Cardiovasc Pharmacol</addtitle><date>2008-09</date><risdate>2008</risdate><volume>52</volume><issue>3</issue><spage>278</spage><epage>285</epage><pages>278-285</pages><issn>0160-2446</issn><eissn>1533-4023</eissn><abstract>To evaluate the mechanisms and the impact of the angiotensin-converting enzyme inhibitor perindopril (P) in a model of doxorubicin (D)-induced cardiotoxicity, male Wistar rats received D (1 mg/kg/d, IP for 10 days), P (2 mg/kg/d by gavage from day 1 to day 18), D (for 10 days) + P (for 18 days) or saline. D decreased systolic blood pressure and body and heart weights. Left ventricular diastolic diameter was increased by D (P < 0.01), but it was not attenuated by P. D decreased plasma vitamin C (P < 0.05) and increased the ascorbyl radical/vitamin C ratio (P < 0.01). This ratio was attenuated by P. No difference was found among groups in cardiac troponin I, brain natriuretic peptide concentrations, and tissue oxidative stress (OS). Myocardial MCP-1 expression was higher in the D group. Cardiac kinin receptor (B1R and B2R) expression was not affected by D, yet binding sites for B2R and B1R were increased in D+P and P groups, respectively (P < 0.05). In conclusion, D induced cardiac functional alterations, inflammation and plasma OS whereas tissue OS, and cardiac kinin receptors expression were not modified. P did not improve cardiac performance, but it modulated kinin receptor expression and enhanced antioxidant defense.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>18806609</pmid><doi>10.1097/FJC.0b013e3181865f28</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-1370-6155</orcidid><orcidid>https://orcid.org/0000-0003-4009-776X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0160-2446 |
| ispartof | Journal of cardiovascular pharmacology, 2008-09, Vol.52 (3), p.278-285 |
| issn | 0160-2446 1533-4023 |
| language | eng |
| recordid | cdi_hal_primary_oai_HAL_hal_03437191v1 |
| source | Ovid Lippincott Williams and Wilkins Journal Legacy Archive; MEDLINE; Journals@Ovid Complete; EZB Electronic Journals Library |
| subjects | Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Antibiotics, Antineoplastic - toxicity Ascorbic Acid - blood Binding Sites Blood Pressure - drug effects Cardiology and cardiovascular system Cardiomyopathies - chemically induced Cardiomyopathies - drug therapy Chemokine CCL2 - metabolism Doxorubicin - toxicity Gene Expression Regulation - drug effects Human health and pathology Life Sciences Male Natriuretic Peptide, Brain - drug effects Natriuretic Peptide, Brain - metabolism Oxidative Stress - drug effects Perindopril - pharmacology Rats Rats, Wistar Receptor, Bradykinin B1 - drug effects Receptor, Bradykinin B1 - metabolism Receptor, Bradykinin B2 - drug effects Receptor, Bradykinin B2 - metabolism Troponin I - drug effects Troponin I - metabolism |
| title | Effects of Angiotensin-1 Converting Enzyme Inhibition on Oxidative Stress and Bradykinin Receptor Expression During Doxorubicin-induced Cardiomyopathy in Rats |
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