Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion
Identifieur interne : 000F53 ( Istex/Corpus ); précédent : 000F52; suivant : 000F54Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion
Auteurs : Silvia G. Ruginsk ; Ernane T. Uchoa ; Lucila Lk Elias ; Jose Antunes-RodriguesSource :
- Clinical and Experimental Pharmacology and Physiology [ 0305-1870 ] ; 2013-10.
Abstract
The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE) in male adult rats. Pretreatment with AEA (100 ng/4 μL) significantly reduced the effect of hypertonic (H‐) EVE on plasma concentrations of prolactin (PRL), oxytocin (OT) and corticosterone, but not vasopressin (AVP). Administration of URB597 (20 μg/5 μL) alone significantly reduced PRL, OT, AVP and corticosterone in the H‐EVE group. Conversely, URB597 and AEA had no significant effect on basal hormone concentrations. Pretreatment with AM251 (200 ng/2 μL) potentiated OT but did not change AVP plasma levels in the H‐EVE group. Hypertonic EVE significantly increased AVP and OT mRNA expression in the supraoptic nucleus (SON), an effect that was blunted in AEA‐pretreated rats. Pretreatment with AEA did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c‐Fos in the SON, but increased nitrate concentrations in the median eminence of animals subjected to H‐EVE. The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by AEA; (ii) activation of CB1R may restrain the response of the neurohypophyseal system (NHS) to EVE; (iii) the hypothalamic–pituitary–adrenal axis, PRL and the NHS may still be sensitive to AEA after EVE, with these effects probably not dependent on AEA metabolism; and (iv) AEA and nitric oxide could interact in vivo as modulators to directly control stress‐induced responses.
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DOI: 10.1111/1440-1681.12155
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title><author><name sortKey="Ruginsk, Silvia G" sort="Ruginsk, Silvia G" uniqKey="Ruginsk S" first="Silvia G" last="Ruginsk">Silvia G. Ruginsk</name><affiliation><mods:affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</mods:affiliation></affiliation></author><author><name sortKey="Uchoa, Ernane T" sort="Uchoa, Ernane T" uniqKey="Uchoa E" first="Ernane T" last="Uchoa">Ernane T. Uchoa</name><affiliation><mods:affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</mods:affiliation></affiliation></author><author><name sortKey="Elias, Lucila Lk" sort="Elias, Lucila Lk" uniqKey="Elias L" first="Lucila Lk" last="Elias">Lucila Lk Elias</name><affiliation><mods:affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</mods:affiliation></affiliation></author><author><name sortKey="Antunes Odrigues, Jose" sort="Antunes Odrigues, Jose" uniqKey="Antunes Odrigues J" first="Jose" last="Antunes-Rodrigues">Jose Antunes-Rodrigues</name><affiliation><mods:affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:1A6A415BF05B6320859946112F8477E6A7294961</idno><date when="2013" year="2013">2013</date><idno type="doi">10.1111/1440-1681.12155</idno><idno type="url">https://api.istex.fr/document/1A6A415BF05B6320859946112F8477E6A7294961/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000F53</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000F53</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title><author><name sortKey="Ruginsk, Silvia G" sort="Ruginsk, Silvia G" uniqKey="Ruginsk S" first="Silvia G" last="Ruginsk">Silvia G. 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Uchoa</name><affiliation><mods:affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</mods:affiliation></affiliation></author><author><name sortKey="Elias, Lucila Lk" sort="Elias, Lucila Lk" uniqKey="Elias L" first="Lucila Lk" last="Elias">Lucila Lk Elias</name><affiliation><mods:affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</mods:affiliation></affiliation></author><author><name sortKey="Antunes Odrigues, Jose" sort="Antunes Odrigues, Jose" uniqKey="Antunes Odrigues J" first="Jose" last="Antunes-Rodrigues">Jose Antunes-Rodrigues</name><affiliation><mods:affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical and Experimental Pharmacology and Physiology</title><title level="j" type="abbrev">Clin Exp Pharmacol Physiol</title><idno type="ISSN">0305-1870</idno><idno type="eISSN">1440-1681</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><date type="published" when="2013-10">2013-10</date><biblScope unit="volume">40</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="698">698</biblScope><biblScope unit="page" to="705">705</biblScope></imprint><idno type="ISSN">0305-1870</idno></series><idno type="istex">1A6A415BF05B6320859946112F8477E6A7294961</idno><idno type="DOI">10.1111/1440-1681.12155</idno><idno type="ArticleID">CEP12155</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0305-1870</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE) in male adult rats. Pretreatment with AEA (100 ng/4 μL) significantly reduced the effect of hypertonic (H‐) EVE on plasma concentrations of prolactin (PRL), oxytocin (OT) and corticosterone, but not vasopressin (AVP). Administration of URB597 (20 μg/5 μL) alone significantly reduced PRL, OT, AVP and corticosterone in the H‐EVE group. Conversely, URB597 and AEA had no significant effect on basal hormone concentrations. Pretreatment with AM251 (200 ng/2 μL) potentiated OT but did not change AVP plasma levels in the H‐EVE group. Hypertonic EVE significantly increased AVP and OT mRNA expression in the supraoptic nucleus (SON), an effect that was blunted in AEA‐pretreated rats. Pretreatment with AEA did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c‐Fos in the SON, but increased nitrate concentrations in the median eminence of animals subjected to H‐EVE. The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by AEA; (ii) activation of CB1R may restrain the response of the neurohypophyseal system (NHS) to EVE; (iii) the hypothalamic–pituitary–adrenal axis, PRL and the NHS may still be sensitive to AEA after EVE, with these effects probably not dependent on AEA metabolism; and (iv) AEA and nitric oxide could interact in vivo as modulators to directly control stress‐induced responses.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Silvia G Ruginsk</name><affiliations><json:string>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</json:string></affiliations></json:item><json:item><name>Ernane T Uchoa</name><affiliations><json:string>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</json:string></affiliations></json:item><json:item><name>Lucila LK Elias</name><affiliations><json:string>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</json:string></affiliations></json:item><json:item><name>Jose Antunes‐Rodrigues</name><affiliations><json:string>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>anandamide</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>corticosterone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>nitric oxide</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oxytocin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>prolactin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>type 1 cannabinoid receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>vasopressin</value></json:item></subject><articleId><json:string>CEP12155</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE) in male adult rats. Pretreatment with AEA (100 ng/4 μL) significantly reduced the effect of hypertonic (H‐) EVE on plasma concentrations of prolactin (PRL), oxytocin (OT) and corticosterone, but not vasopressin (AVP). Administration of URB597 (20 μg/5 μL) alone significantly reduced PRL, OT, AVP and corticosterone in the H‐EVE group. Conversely, URB597 and AEA had no significant effect on basal hormone concentrations. Pretreatment with AM251 (200 ng/2 μL) potentiated OT but did not change AVP plasma levels in the H‐EVE group. Hypertonic EVE significantly increased AVP and OT mRNA expression in the supraoptic nucleus (SON), an effect that was blunted in AEA‐pretreated rats. Pretreatment with AEA did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c‐Fos in the SON, but increased nitrate concentrations in the median eminence of animals subjected to H‐EVE. The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by AEA; (ii) activation of CB1R may restrain the response of the neurohypophyseal system (NHS) to EVE; (iii) the hypothalamic–pituitary–adrenal axis, PRL and the NHS may still be sensitive to AEA after EVE, with these effects probably not dependent on AEA metabolism; and (iv) AEA and nitric oxide could interact in vivo as modulators to directly control stress‐induced responses.</abstract><qualityIndicators><score>9.928</score><pdfVersion>1.7</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1694</abstractCharCount><pdfWordCount>5366</pdfWordCount><pdfCharCount>32212</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>244</abstractWordCount></qualityIndicators><title>Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title><genre><json:string>article</json:string></genre><host><volume>40</volume><publisherId><json:string>CEP</json:string></publisherId><pages><total>8</total><last>705</last><first>698</first></pages><issn><json:string>0305-1870</json:string></issn><issue>10</issue><subject><json:item><value>Original Article</value></json:item></subject><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1440-1681</json:string></eissn><title>Clinical and Experimental Pharmacology and Physiology</title><doi><json:string>10.1111/(ISSN)1440-1681</json:string></doi></host><publicationDate>2013</publicationDate><copyrightDate>2013</copyrightDate><doi><json:string>10.1111/1440-1681.12155</json:string></doi><id>1A6A415BF05B6320859946112F8477E6A7294961</id><score>0.050984934</score><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/1A6A415BF05B6320859946112F8477E6A7294961/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/1A6A415BF05B6320859946112F8477E6A7294961/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/1A6A415BF05B6320859946112F8477E6A7294961/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><availability><p>Copyright © 2013 Wiley Publishing Asia Pty Ltd© 2013 Wiley Publishing Asia Pty Ltd</p></availability><date>2013-08-13</date></publicationStmt><notesStmt><note>Fundacao de Amparo a Pesquisa do Estado de Sao Paulo - No. 2006/51938–5;</note><note>Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - No. 143175/2008–4;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title><author xml:id="author-1"><persName><forename type="first">Silvia G</forename><surname>Ruginsk</surname></persName><note type="correspondence"><p>Correspondence: Silvia Graciela Ruginsk, Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, 3900 Bandeirantes Avenue, 14049–900 Ribeirao Preto, Sao Paulo, Brazil. Email:</p></note><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation></author><author xml:id="author-2"><persName><forename type="first">Ernane T</forename><surname>Uchoa</surname></persName><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation></author><author xml:id="author-3"><persName><forename type="first">Lucila LK</forename><surname>Elias</surname></persName><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation></author><author xml:id="author-4"><persName><forename type="first">Jose</forename><surname>Antunes‐Rodrigues</surname></persName><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation></author></analytic><monogr><title level="j">Clinical and Experimental Pharmacology and Physiology</title><title level="j" type="abbrev">Clin Exp Pharmacol Physiol</title><idno type="pISSN">0305-1870</idno><idno type="eISSN">1440-1681</idno><idno type="DOI">10.1111/(ISSN)1440-1681</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><date type="published" when="2013-10"></date><biblScope unit="volume">40</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="698">698</biblScope><biblScope unit="page" to="705">705</biblScope></imprint></monogr><idno type="istex">1A6A415BF05B6320859946112F8477E6A7294961</idno><idno type="DOI">10.1111/1440-1681.12155</idno><idno type="ArticleID">CEP12155</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2013-08-13</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE) in male adult rats. Pretreatment with AEA (100 ng/4 μL) significantly reduced the effect of hypertonic (H‐) EVE on plasma concentrations of prolactin (PRL), oxytocin (OT) and corticosterone, but not vasopressin (AVP). Administration of URB597 (20 μg/5 μL) alone significantly reduced PRL, OT, AVP and corticosterone in the H‐EVE group. Conversely, URB597 and AEA had no significant effect on basal hormone concentrations. Pretreatment with AM251 (200 ng/2 μL) potentiated OT but did not change AVP plasma levels in the H‐EVE group. Hypertonic EVE significantly increased AVP and OT mRNA expression in the supraoptic nucleus (SON), an effect that was blunted in AEA‐pretreated rats. Pretreatment with AEA did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c‐Fos in the SON, but increased nitrate concentrations in the median eminence of animals subjected to H‐EVE. The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by AEA; (ii) activation of CB1R may restrain the response of the neurohypophyseal system (NHS) to EVE; (iii) the hypothalamic–pituitary–adrenal axis, PRL and the NHS may still be sensitive to AEA after EVE, with these effects probably not dependent on AEA metabolism; and (iv) AEA and nitric oxide could interact in vivo as modulators to directly control stress‐induced responses.</p></abstract><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>anandamide</term></item><item><term>corticosterone</term></item><item><term>nitric oxide</term></item><item><term>oxytocin</term></item><item><term>prolactin</term></item><item><term>type 1 cannabinoid receptor</term></item><item><term>vasopressin</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2013-01-30">Received</change><change when="2013-07-17">Registration</change><change when="2013-08-13">Created</change><change when="2013-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/1A6A415BF05B6320859946112F8477E6A7294961/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="cep12155" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1440-1681</doi><issn type="print">0305-1870</issn><issn type="electronic">1440-1681</issn><idGroup><id type="product" value="CEP"></id></idGroup><titleGroup><title sort="CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY" type="main">Clinical and Experimental Pharmacology and Physiology</title><title type="short">Clin Exp Pharmacol Physiol</title></titleGroup></publicationMeta><publicationMeta level="part" position="100"><doi origin="wiley">10.1111/cep.2013.40.issue-10</doi><copyright ownership="publisher">Copyright © 2013 Wiley Publishing Asia Pty Ltd</copyright><numberingGroup><numbering number="40" type="journalVolume">40</numbering><numbering type="journalIssue">10</numbering></numberingGroup><coverDate startDate="2013-10">October 2013</coverDate></publicationMeta><publicationMeta level="unit" position="40" status="forIssue" type="article"><doi>10.1111/1440-1681.12155</doi><idGroup><id type="unit" value="CEP12155"></id></idGroup><countGroup><count number="8" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="publisher">© 2013 Wiley Publishing Asia Pty Ltd</copyright><eventGroup><event date="2013-01-30" type="manuscriptReceived"></event><event date="2013-06-10" type="manuscriptRevised"></event><event date="2013-07-17" type="manuscriptAccepted"></event><event agent="SPS" date="2013-08-13" type="xmlCreated"></event><event type="publishedOnlineAccepted" date="2013-07-23"></event><event type="firstOnline" date="2013-09-23"></event><event type="publishedOnlineFinalForm" date="2013-09-23"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-09"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-03"></event></eventGroup><numberingGroup><numbering type="pageFirst">698</numbering><numbering type="pageLast">705</numbering></numberingGroup><correspondenceTo>Correspondence: Silvia Graciela Ruginsk, Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, 3900 Bandeirantes Avenue, 14049–900 Ribeirao Preto, Sao Paulo, Brazil. Email: <email>sruginsk@rfi.fmrp.usp.br</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CEP.CEP12155.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title><title type="shortAuthors"><i>SG Ruginsk</i> et al.</title></titleGroup><creators><creator affiliationRef="#cep12155-aff-0001" corresponding="yes" creatorRole="author" xml:id="cep12155-cr-0001"><personName><givenNames>Silvia G</givenNames> <familyName>Ruginsk</familyName></personName></creator><creator affiliationRef="#cep12155-aff-0001" creatorRole="author" xml:id="cep12155-cr-0002"><personName><givenNames>Ernane T</givenNames> <familyName>Uchoa</familyName></personName></creator><creator affiliationRef="#cep12155-aff-0001" creatorRole="author" xml:id="cep12155-cr-0003"><personName><givenNames>Lucila LK</givenNames> <familyName>Elias</familyName></personName></creator><creator affiliationRef="#cep12155-aff-0001" creatorRole="author" xml:id="cep12155-cr-0004"><personName><givenNames>Jose</givenNames> <familyName>Antunes‐Rodrigues</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="BR" type="organization" xml:id="cep12155-aff-0001"><orgDiv>Department of Physiology</orgDiv> <orgName>School of Medicine of Ribeirao Preto</orgName> <orgName>University of Sao Paulo</orgName> <address><city>Sao Paulo</city> <countryPart>SP</countryPart> <country>Brazil</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="cep12155-kwd-0001">anandamide</keyword><keyword xml:id="cep12155-kwd-0002">corticosterone</keyword><keyword xml:id="cep12155-kwd-0003">nitric oxide</keyword><keyword xml:id="cep12155-kwd-0004">oxytocin</keyword><keyword xml:id="cep12155-kwd-0005">prolactin</keyword><keyword xml:id="cep12155-kwd-0006">type 1 cannabinoid receptor</keyword><keyword xml:id="cep12155-kwd-0007">vasopressin</keyword></keywordGroup><fundingInfo><fundingAgency>Fundacao de Amparo a Pesquisa do Estado de Sao Paulo</fundingAgency><fundingNumber>2006/51938–5</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Conselho Nacional de Desenvolvimento Cientifico e Tecnologico </fundingAgency><fundingNumber>143175/2008–4</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:id="cep12155-abs-0001"><title type="main">Summary</title><p><list formatted="paragraph" style="1" xml:id="cep12155-list-0001"><listItem>The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (<fc>AEA</fc>), an inhibitor of fatty acid amide hydrolase activity (<fc>URB</fc>597) and a <fc>CB</fc><sub>1</sub> receptor (<fc>CB</fc><sub>1</sub><fc>R</fc>) antagonist (<fc>AM</fc>251) on the homeostatic responses elicited by extracellular volume expansion (<fc>EVE</fc>) in male adult rats.</listItem><listItem>Pretreatment with <fc>AEA</fc> (100 ng/4 μL) significantly reduced the effect of hypertonic (H‐) <fc>EVE</fc> on plasma concentrations of prolactin (<fc>PRL</fc>), oxytocin (<fc>OT</fc>) and corticosterone, but not vasopressin (<fc>AVP</fc>). Administration of <fc>URB</fc>597 (20 μg/5 μL) alone significantly reduced <fc>PRL</fc>,<fc> OT</fc>,<fc> AVP</fc> and corticosterone in the <fc>H</fc>‐<fc>EVE</fc> group. Conversely, <fc>URB</fc>597 and <fc>AEA</fc> had no significant effect on basal hormone concentrations. Pretreatment with <fc>AM</fc>251 (200 ng/2 μL) potentiated <fc>OT</fc> but did not change <fc>AVP</fc> plasma levels in the <fc>H</fc>‐<fc>EVE</fc> group.</listItem><listItem>Hypertonic <fc>EVE</fc> significantly increased <i>AVP</i> and <i>OT </i><fc>mRNA</fc> expression in the supraoptic nucleus (<fc>SON</fc>), an effect that was blunted in <fc>AEA</fc>‐pretreated rats. Pretreatment with <fc>AEA</fc> did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c‐<fc>F</fc>os in the <fc>SON</fc>, but increased nitrate concentrations in the median eminence of animals subjected to <fc>H‐EVE.</fc></listItem><listItem>The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by <fc>AEA</fc>; (ii) activation of <fc>CB</fc><sub>1</sub>R may restrain the response of the neurohypophyseal system (<fc>NHS</fc>) to <fc>EVE</fc>; (iii) the hypothalamic–pituitary–adrenal axis, <fc>PRL</fc> and the <fc>NHS</fc> may still be sensitive to <fc>AEA</fc> after <fc>EVE</fc>, with these effects probably not dependent on <fc>AEA</fc> metabolism; and (iv) <fc>AEA</fc> and nitric oxide could interact <i>in vivo</i> as modulators to directly control stress‐induced responses.</listItem></list></p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion</title></titleInfo><name type="personal"><namePart type="given">Silvia G</namePart><namePart type="family">Ruginsk</namePart><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation><description>Correspondence: Silvia Graciela Ruginsk, Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, 3900 Bandeirantes Avenue, 14049–900 Ribeirao Preto, Sao Paulo, Brazil. Email: </description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ernane T</namePart><namePart type="family">Uchoa</namePart><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lucila LK</namePart><namePart type="family">Elias</namePart><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jose</namePart><namePart type="family">Antunes‐Rodrigues</namePart><affiliation>Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, SP, Sao Paulo, Brazil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2013-10</dateIssued><dateCreated encoding="w3cdtf">2013-08-13</dateCreated><dateCaptured encoding="w3cdtf">2013-01-30</dateCaptured><dateValid encoding="w3cdtf">2013-07-17</dateValid><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>The aim of the present study was to evaluate the effects of intracerebroventricular administration of anandamide (AEA), an inhibitor of fatty acid amide hydrolase activity (URB597) and a CB1 receptor (CB1R) antagonist (AM251) on the homeostatic responses elicited by extracellular volume expansion (EVE) in male adult rats. Pretreatment with AEA (100 ng/4 μL) significantly reduced the effect of hypertonic (H‐) EVE on plasma concentrations of prolactin (PRL), oxytocin (OT) and corticosterone, but not vasopressin (AVP). Administration of URB597 (20 μg/5 μL) alone significantly reduced PRL, OT, AVP and corticosterone in the H‐EVE group. Conversely, URB597 and AEA had no significant effect on basal hormone concentrations. Pretreatment with AM251 (200 ng/2 μL) potentiated OT but did not change AVP plasma levels in the H‐EVE group. Hypertonic EVE significantly increased AVP and OT mRNA expression in the supraoptic nucleus (SON), an effect that was blunted in AEA‐pretreated rats. Pretreatment with AEA did not change the percentage of vasopressinergic or oxytocinergic neurons colocalizing c‐Fos in the SON, but increased nitrate concentrations in the median eminence of animals subjected to H‐EVE. The present data suggest that: (i) vasopressinergic and oxytocinergic neurons may be differentially affected by AEA; (ii) activation of CB1R may restrain the response of the neurohypophyseal system (NHS) to EVE; (iii) the hypothalamic–pituitary–adrenal axis, PRL and the NHS may still be sensitive to AEA after EVE, with these effects probably not dependent on AEA metabolism; and (iv) AEA and nitric oxide could interact in vivo as modulators to directly control stress‐induced responses.</abstract><note type="funding">Fundacao de Amparo a Pesquisa do Estado de Sao Paulo - No. 2006/51938–5; </note><note type="funding">Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - No. 143175/2008–4; </note><subject><genre>keywords</genre><topic>anandamide</topic><topic>corticosterone</topic><topic>nitric oxide</topic><topic>oxytocin</topic><topic>prolactin</topic><topic>type 1 cannabinoid receptor</topic><topic>vasopressin</topic></subject><relatedItem type="host"><titleInfo><title>Clinical and Experimental Pharmacology and Physiology</title></titleInfo><titleInfo type="abbreviated"><title>Clin Exp Pharmacol Physiol</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0305-1870</identifier><identifier type="eISSN">1440-1681</identifier><identifier type="DOI">10.1111/(ISSN)1440-1681</identifier><identifier type="PublisherID">CEP</identifier><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>698</start><end>705</end><total>8</total></extent></part></relatedItem><identifier type="istex">1A6A415BF05B6320859946112F8477E6A7294961</identifier><identifier type="DOI">10.1111/1440-1681.12155</identifier><identifier type="ArticleID">CEP12155</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2013 Wiley Publishing Asia Pty Ltd© 2013 Wiley Publishing Asia Pty Ltd</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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