Cardiac capsaicin‐sensitive sensory nerves regulate myocardial relaxation via S‐nitrosylation of SERCA: role of peroxynitrite
Background and purpose: Sensory neuropathy develops in the presence of cardiovascular risk factors (e.g. diabetes, dyslipidemia), but its pathological consequences in the heart are unclear. We have previously shown that systemic sensory chemodenervation by capsaicin leads to impaired myocardial rela...
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| Veröffentlicht in: | British journal of pharmacology 2008-02, Vol.153 (3), p.488-496 |
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| creator | Bencsik, P Kupai, K Giricz, Z Görbe, A Huliák, I Fürst, S Dux, L Csont, T Jancsó, G Ferdinandy, P |
| description | Background and purpose:
Sensory neuropathy develops in the presence of cardiovascular risk factors (e.g. diabetes, dyslipidemia), but its pathological consequences in the heart are unclear. We have previously shown that systemic sensory chemodenervation by capsaicin leads to impaired myocardial relaxation and diminished cardiac nitric oxide (NO) content. Here we examined the mechanism of diminished NO formation and if it may lead to a reduction of peroxynitrite (ONOO−)‐induced S‐nitrosylation of sarcoendoplasmic reticulum Ca2+‐ATPase (SERCA2a).
Experimental approach:
Male Wistar rats were treated with capsaicin for 3 days to induce sensory chemodenervation. Seven days later, myocardial function and biochemical parameters were measured.
Key results:
Capsaicin pretreatment significantly increased left ventricular end‐diastolic pressure (LVEDP) decreased cardiac NO level, Ca2+‐dependent NO synthase (NOS) activity, and NOS‐3 mRNA. Myocardial superoxide content, xanthine oxidoreductase and NADPH oxidase activities did not change, although superoxide dismutase (SOD) activity increased. Myocardial and serum ONOO− concentration and S‐nitrosylation of SERCA2a were significantly decreased.
Conclusions and implications:
Our results show that sensory chemodenervation decreases cardiac NO via decreased expression and activity of Ca2+‐dependent NOS and increases SOD activity, thereby leading to decreased basal ONOO− formation and reduction of S‐nitrosylation of SERCA2a, which causes impaired myocardial relaxation characterized by increased left ventricular end‐diastolic pressure (LVEDP). This suggests that capsaicin sensitive sensory neurons regulate myocardial relaxation via maintaining basal ONOO− formation and SERCA S‐nitrosylation.
British Journal of Pharmacology (2008) 153, 488–496; doi:10.1038/sj.bjp.0707599; published online 26 November 2007 |
| doi_str_mv | 10.1038/sj.bjp.0707599 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2241783</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70259526</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4885-14f6c757f792efbfc596104ec2928465c5b08c7e52c2aab7c12dae3a963154953</originalsourceid><addsrcrecordid>eNqFkc9u1DAQxiMEotvClSOKkOCWxXbi2OaAVFaFIlUCUThbjndSHHntYCdLcytvwDPyJDhsVP5cONme-c034_my7BFGa4xK_jx266br14ghRoW4k61wxeqClhzfzVYIIVZgzPlRdhxjh1BKMno_O8IclUwgvsq-bVTYGqVzrfqojDbux833CC6awewhn28-TLmDsIeYB7garRog301e_yq0KWbVtRqMd_neqPwy1TszBB8ne4j6Nr88-7A5fZEHb2F-9hD89TRTZoAH2b1W2QgPl_Mk-_T67OPmvLh49-bt5vSi0BXntMBVW2tGWcsEgbZpNRU1RhVoIgivaqppg7hmQIkmSjVMY7JVUCpRl5hWgpYn2cuDbj82O9hqcENQVvbB7FSYpFdG_p1x5rO88ntJSIUZL5PAs0Ug-C8jxEHuTNRgrXLgxygZIlRQUifwyT9g58fg0uckwYwgSkWVoPUB0mlVMUB7OwlGcrZWxk4ma-VibSp4_Of8v_HFywQ8XQAVtbJtUE6beMuR5H5Zink8cuC-GgvTf9rKV-_P67S9n-a8woY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>217205594</pqid></control><display><type>article</type><title>Cardiac capsaicin‐sensitive sensory nerves regulate myocardial relaxation via S‐nitrosylation of SERCA: role of peroxynitrite</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Wiley Free Content</source><source>Wiley Online Library All Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Bencsik, P ; Kupai, K ; Giricz, Z ; Görbe, A ; Huliák, I ; Fürst, S ; Dux, L ; Csont, T ; Jancsó, G ; Ferdinandy, P</creator><creatorcontrib>Bencsik, P ; Kupai, K ; Giricz, Z ; Görbe, A ; Huliák, I ; Fürst, S ; Dux, L ; Csont, T ; Jancsó, G ; Ferdinandy, P</creatorcontrib><description>Background and purpose:
Sensory neuropathy develops in the presence of cardiovascular risk factors (e.g. diabetes, dyslipidemia), but its pathological consequences in the heart are unclear. We have previously shown that systemic sensory chemodenervation by capsaicin leads to impaired myocardial relaxation and diminished cardiac nitric oxide (NO) content. Here we examined the mechanism of diminished NO formation and if it may lead to a reduction of peroxynitrite (ONOO−)‐induced S‐nitrosylation of sarcoendoplasmic reticulum Ca2+‐ATPase (SERCA2a).
Experimental approach:
Male Wistar rats were treated with capsaicin for 3 days to induce sensory chemodenervation. Seven days later, myocardial function and biochemical parameters were measured.
Key results:
Capsaicin pretreatment significantly increased left ventricular end‐diastolic pressure (LVEDP) decreased cardiac NO level, Ca2+‐dependent NO synthase (NOS) activity, and NOS‐3 mRNA. Myocardial superoxide content, xanthine oxidoreductase and NADPH oxidase activities did not change, although superoxide dismutase (SOD) activity increased. Myocardial and serum ONOO− concentration and S‐nitrosylation of SERCA2a were significantly decreased.
Conclusions and implications:
Our results show that sensory chemodenervation decreases cardiac NO via decreased expression and activity of Ca2+‐dependent NOS and increases SOD activity, thereby leading to decreased basal ONOO− formation and reduction of S‐nitrosylation of SERCA2a, which causes impaired myocardial relaxation characterized by increased left ventricular end‐diastolic pressure (LVEDP). This suggests that capsaicin sensitive sensory neurons regulate myocardial relaxation via maintaining basal ONOO− formation and SERCA S‐nitrosylation.
British Journal of Pharmacology (2008) 153, 488–496; doi:10.1038/sj.bjp.0707599; published online 26 November 2007</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0707599</identifier><identifier>PMID: 18037908</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biological and medical sciences ; Calcium - metabolism ; capsaicin ; Capsaicin - pharmacology ; free radicals ; Male ; Medical sciences ; myocardial function ; Myocardium - metabolism ; Neurons, Afferent - drug effects ; Neurons, Afferent - metabolism ; nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - drug effects ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type III - drug effects ; Nitric Oxide Synthase Type III - metabolism ; peroxynitrite ; Peroxynitrous Acid - metabolism ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; Research Papers ; RNA, Messenger - metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - drug effects ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism ; sensory nerves ; SERCA ; Superoxide Dismutase - drug effects ; Superoxide Dismutase - metabolism ; S‐nitrosylation ; Ventricular Function, Left - drug effects</subject><ispartof>British journal of pharmacology, 2008-02, Vol.153 (3), p.488-496</ispartof><rights>2008 British Pharmacological Society</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 2008</rights><rights>Copyright 2008, Nature Publishing Group 2008 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4885-14f6c757f792efbfc596104ec2928465c5b08c7e52c2aab7c12dae3a963154953</citedby><cites>FETCH-LOGICAL-c4885-14f6c757f792efbfc596104ec2928465c5b08c7e52c2aab7c12dae3a963154953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2241783/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2241783/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1416,1432,27923,27924,45573,45574,46408,46832,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20143396$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18037908$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bencsik, P</creatorcontrib><creatorcontrib>Kupai, K</creatorcontrib><creatorcontrib>Giricz, Z</creatorcontrib><creatorcontrib>Görbe, A</creatorcontrib><creatorcontrib>Huliák, I</creatorcontrib><creatorcontrib>Fürst, S</creatorcontrib><creatorcontrib>Dux, L</creatorcontrib><creatorcontrib>Csont, T</creatorcontrib><creatorcontrib>Jancsó, G</creatorcontrib><creatorcontrib>Ferdinandy, P</creatorcontrib><title>Cardiac capsaicin‐sensitive sensory nerves regulate myocardial relaxation via S‐nitrosylation of SERCA: role of peroxynitrite</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and purpose:
Sensory neuropathy develops in the presence of cardiovascular risk factors (e.g. diabetes, dyslipidemia), but its pathological consequences in the heart are unclear. We have previously shown that systemic sensory chemodenervation by capsaicin leads to impaired myocardial relaxation and diminished cardiac nitric oxide (NO) content. Here we examined the mechanism of diminished NO formation and if it may lead to a reduction of peroxynitrite (ONOO−)‐induced S‐nitrosylation of sarcoendoplasmic reticulum Ca2+‐ATPase (SERCA2a).
Experimental approach:
Male Wistar rats were treated with capsaicin for 3 days to induce sensory chemodenervation. Seven days later, myocardial function and biochemical parameters were measured.
Key results:
Capsaicin pretreatment significantly increased left ventricular end‐diastolic pressure (LVEDP) decreased cardiac NO level, Ca2+‐dependent NO synthase (NOS) activity, and NOS‐3 mRNA. Myocardial superoxide content, xanthine oxidoreductase and NADPH oxidase activities did not change, although superoxide dismutase (SOD) activity increased. Myocardial and serum ONOO− concentration and S‐nitrosylation of SERCA2a were significantly decreased.
Conclusions and implications:
Our results show that sensory chemodenervation decreases cardiac NO via decreased expression and activity of Ca2+‐dependent NOS and increases SOD activity, thereby leading to decreased basal ONOO− formation and reduction of S‐nitrosylation of SERCA2a, which causes impaired myocardial relaxation characterized by increased left ventricular end‐diastolic pressure (LVEDP). This suggests that capsaicin sensitive sensory neurons regulate myocardial relaxation via maintaining basal ONOO− formation and SERCA S‐nitrosylation.
British Journal of Pharmacology (2008) 153, 488–496; doi:10.1038/sj.bjp.0707599; published online 26 November 2007</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - metabolism</subject><subject>capsaicin</subject><subject>Capsaicin - pharmacology</subject><subject>free radicals</subject><subject>Male</subject><subject>Medical sciences</subject><subject>myocardial function</subject><subject>Myocardium - metabolism</subject><subject>Neurons, Afferent - drug effects</subject><subject>Neurons, Afferent - metabolism</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - drug effects</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type III - drug effects</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>peroxynitrite</subject><subject>Peroxynitrous Acid - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Research Papers</subject><subject>RNA, Messenger - metabolism</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - drug effects</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</subject><subject>sensory nerves</subject><subject>SERCA</subject><subject>Superoxide Dismutase - drug effects</subject><subject>Superoxide Dismutase - metabolism</subject><subject>S‐nitrosylation</subject><subject>Ventricular Function, Left - drug effects</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc9u1DAQxiMEotvClSOKkOCWxXbi2OaAVFaFIlUCUThbjndSHHntYCdLcytvwDPyJDhsVP5cONme-c034_my7BFGa4xK_jx266br14ghRoW4k61wxeqClhzfzVYIIVZgzPlRdhxjh1BKMno_O8IclUwgvsq-bVTYGqVzrfqojDbux833CC6awewhn28-TLmDsIeYB7garRog301e_yq0KWbVtRqMd_neqPwy1TszBB8ne4j6Nr88-7A5fZEHb2F-9hD89TRTZoAH2b1W2QgPl_Mk-_T67OPmvLh49-bt5vSi0BXntMBVW2tGWcsEgbZpNRU1RhVoIgivaqppg7hmQIkmSjVMY7JVUCpRl5hWgpYn2cuDbj82O9hqcENQVvbB7FSYpFdG_p1x5rO88ntJSIUZL5PAs0Ug-C8jxEHuTNRgrXLgxygZIlRQUifwyT9g58fg0uckwYwgSkWVoPUB0mlVMUB7OwlGcrZWxk4ma-VibSp4_Of8v_HFywQ8XQAVtbJtUE6beMuR5H5Zink8cuC-GgvTf9rKV-_P67S9n-a8woY</recordid><startdate>200802</startdate><enddate>200802</enddate><creator>Bencsik, P</creator><creator>Kupai, K</creator><creator>Giricz, Z</creator><creator>Görbe, A</creator><creator>Huliák, I</creator><creator>Fürst, S</creator><creator>Dux, L</creator><creator>Csont, T</creator><creator>Jancsó, G</creator><creator>Ferdinandy, P</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200802</creationdate><title>Cardiac capsaicin‐sensitive sensory nerves regulate myocardial relaxation via S‐nitrosylation of SERCA: role of peroxynitrite</title><author>Bencsik, P ; Kupai, K ; Giricz, Z ; Görbe, A ; Huliák, I ; Fürst, S ; Dux, L ; Csont, T ; Jancsó, G ; Ferdinandy, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4885-14f6c757f792efbfc596104ec2928465c5b08c7e52c2aab7c12dae3a963154953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - metabolism</topic><topic>capsaicin</topic><topic>Capsaicin - pharmacology</topic><topic>free radicals</topic><topic>Male</topic><topic>Medical sciences</topic><topic>myocardial function</topic><topic>Myocardium - metabolism</topic><topic>Neurons, Afferent - drug effects</topic><topic>Neurons, Afferent - metabolism</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - drug effects</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type III - drug effects</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>peroxynitrite</topic><topic>Peroxynitrous Acid - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Research Papers</topic><topic>RNA, Messenger - metabolism</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - drug effects</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</topic><topic>sensory nerves</topic><topic>SERCA</topic><topic>Superoxide Dismutase - drug effects</topic><topic>Superoxide Dismutase - metabolism</topic><topic>S‐nitrosylation</topic><topic>Ventricular Function, Left - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bencsik, P</creatorcontrib><creatorcontrib>Kupai, K</creatorcontrib><creatorcontrib>Giricz, Z</creatorcontrib><creatorcontrib>Görbe, A</creatorcontrib><creatorcontrib>Huliák, I</creatorcontrib><creatorcontrib>Fürst, S</creatorcontrib><creatorcontrib>Dux, L</creatorcontrib><creatorcontrib>Csont, T</creatorcontrib><creatorcontrib>Jancsó, G</creatorcontrib><creatorcontrib>Ferdinandy, P</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bencsik, P</au><au>Kupai, K</au><au>Giricz, Z</au><au>Görbe, A</au><au>Huliák, I</au><au>Fürst, S</au><au>Dux, L</au><au>Csont, T</au><au>Jancsó, G</au><au>Ferdinandy, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac capsaicin‐sensitive sensory nerves regulate myocardial relaxation via S‐nitrosylation of SERCA: role of peroxynitrite</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2008-02</date><risdate>2008</risdate><volume>153</volume><issue>3</issue><spage>488</spage><epage>496</epage><pages>488-496</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Background and purpose:
Sensory neuropathy develops in the presence of cardiovascular risk factors (e.g. diabetes, dyslipidemia), but its pathological consequences in the heart are unclear. We have previously shown that systemic sensory chemodenervation by capsaicin leads to impaired myocardial relaxation and diminished cardiac nitric oxide (NO) content. Here we examined the mechanism of diminished NO formation and if it may lead to a reduction of peroxynitrite (ONOO−)‐induced S‐nitrosylation of sarcoendoplasmic reticulum Ca2+‐ATPase (SERCA2a).
Experimental approach:
Male Wistar rats were treated with capsaicin for 3 days to induce sensory chemodenervation. Seven days later, myocardial function and biochemical parameters were measured.
Key results:
Capsaicin pretreatment significantly increased left ventricular end‐diastolic pressure (LVEDP) decreased cardiac NO level, Ca2+‐dependent NO synthase (NOS) activity, and NOS‐3 mRNA. Myocardial superoxide content, xanthine oxidoreductase and NADPH oxidase activities did not change, although superoxide dismutase (SOD) activity increased. Myocardial and serum ONOO− concentration and S‐nitrosylation of SERCA2a were significantly decreased.
Conclusions and implications:
Our results show that sensory chemodenervation decreases cardiac NO via decreased expression and activity of Ca2+‐dependent NOS and increases SOD activity, thereby leading to decreased basal ONOO− formation and reduction of S‐nitrosylation of SERCA2a, which causes impaired myocardial relaxation characterized by increased left ventricular end‐diastolic pressure (LVEDP). This suggests that capsaicin sensitive sensory neurons regulate myocardial relaxation via maintaining basal ONOO− formation and SERCA S‐nitrosylation.
British Journal of Pharmacology (2008) 153, 488–496; doi:10.1038/sj.bjp.0707599; published online 26 November 2007</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>18037908</pmid><doi>10.1038/sj.bjp.0707599</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Calcium - metabolism capsaicin Capsaicin - pharmacology free radicals Male Medical sciences myocardial function Myocardium - metabolism Neurons, Afferent - drug effects Neurons, Afferent - metabolism nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase - drug effects Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type III - drug effects Nitric Oxide Synthase Type III - metabolism peroxynitrite Peroxynitrous Acid - metabolism Pharmacology. Drug treatments Rats Rats, Wistar Research Papers RNA, Messenger - metabolism Sarcoplasmic Reticulum Calcium-Transporting ATPases - drug effects Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism sensory nerves SERCA Superoxide Dismutase - drug effects Superoxide Dismutase - metabolism S‐nitrosylation Ventricular Function, Left - drug effects |
| title | Cardiac capsaicin‐sensitive sensory nerves regulate myocardial relaxation via S‐nitrosylation of SERCA: role of peroxynitrite |
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