Short-term estradiol treatment enhances pituitary-adrenal axis and sympathetic responses to psychosocial stress in healthy young men.
Identifieur interne : 000950 ( PubMed/Corpus ); précédent : 000949; suivant : 000951Short-term estradiol treatment enhances pituitary-adrenal axis and sympathetic responses to psychosocial stress in healthy young men.
Auteurs : C. Kirschbaum ; N. Schommer ; I. Federenko ; J. Gaab ; O. Neumann ; M. Oellers ; N. Rohleder ; A. Untiedt ; J. Hanker ; K M Pirke ; D H HellhammerSource :
- The Journal of clinical endocrinology and metabolism [ 0021-972X ] ; 1996.
English descriptors
- KwdEn :
- Adrenal Glands (physiology), Adrenocorticotropic Hormone (blood), Adult, Estradiol (administration & dosage), Estradiol (therapeutic use), Heart Rate, Humans, Hydrocortisone (blood), Kinetics, Male, Norepinephrine (blood), Pituitary Gland (physiology), Stress, Psychological (drug therapy), Stress, Psychological (physiopathology), Sympathetic Nervous System (physiopathology).
- MESH :
- chemical , administration & dosage : Estradiol.
- chemical , blood : Adrenocorticotropic Hormone, Hydrocortisone, Norepinephrine.
- drug therapy : Stress, Psychological.
- physiology : Adrenal Glands, Pituitary Gland.
- physiopathology : Stress, Psychological, Sympathetic Nervous System.
- chemical , therapeutic use : Estradiol.
- Adult, Heart Rate, Humans, Kinetics, Male.
Abstract
Evidence from animal studies and clinical observations suggest that the activity of the pituitary-adrenal axis is under significant influence of sex steroids. The present study investigated how a short term elevation of estradiol levels affects ACTH, cortisol, norepinephrine, and heart rate responses to mental stress in healthy men. In a double blind study, 16 men received a patch delivering 0.1 mg estradiol/day transdermally, and age- and body mass index-matched control subjects received a placebo patch. Twenty-four to 48 h later, they were exposed to a brief psychosocial stressor (free speech and mental arithmetic in front of an audience). In response to the psychosocial stressor, ACTH, cortisol, norepinephrine, and heart rate were increased in both experimental groups (all P < 0.0001). However, the estradiol-treated subjects showed exaggerated peak ACTH (P < 0.001) and cortisol (P < 0.002) responses compared to the placebo group. Also, the norepinephrine area under the response curve was greater in the estradiol group (P < 0.05). Although heart rate responses differences failed to reach statistical significance, they, too, tended to be larger in the estradiol group. Neither mood ratings before or after the stressor, nor ratings of the perception of the stressor could explain the observed endocrine response differences. In conclusion, short term estradiol administration resulted in hyperresponses of the pituitary-adrenal axis and norepinephrine to psychosocial stress in healthy young men independent of psychological effects, as assessed in this study.
DOI: 10.1210/jcem.81.10.8855815
PubMed: 8855815
Links to Exploration step
pubmed:8855815Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Short-term estradiol treatment enhances pituitary-adrenal axis and sympathetic responses to psychosocial stress in healthy young men.</title><author><name sortKey="Kirschbaum, C" sort="Kirschbaum, C" uniqKey="Kirschbaum C" first="C" last="Kirschbaum">C. Kirschbaum</name><affiliation><nlm:affiliation>Center for Psychobiological, University of Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Schommer, N" sort="Schommer, N" uniqKey="Schommer N" first="N" last="Schommer">N. Schommer</name></author><author><name sortKey="Federenko, I" sort="Federenko, I" uniqKey="Federenko I" first="I" last="Federenko">I. Federenko</name></author><author><name sortKey="Gaab, J" sort="Gaab, J" uniqKey="Gaab J" first="J" last="Gaab">J. Gaab</name></author><author><name sortKey="Neumann, O" sort="Neumann, O" uniqKey="Neumann O" first="O" last="Neumann">O. Neumann</name></author><author><name sortKey="Oellers, M" sort="Oellers, M" uniqKey="Oellers M" first="M" last="Oellers">M. Oellers</name></author><author><name sortKey="Rohleder, N" sort="Rohleder, N" uniqKey="Rohleder N" first="N" last="Rohleder">N. Rohleder</name></author><author><name sortKey="Untiedt, A" sort="Untiedt, A" uniqKey="Untiedt A" first="A" last="Untiedt">A. Untiedt</name></author><author><name sortKey="Hanker, J" sort="Hanker, J" uniqKey="Hanker J" first="J" last="Hanker">J. Hanker</name></author><author><name sortKey="Pirke, K M" sort="Pirke, K M" uniqKey="Pirke K" first="K M" last="Pirke">K M Pirke</name></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D H" last="Hellhammer">D H Hellhammer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8855815</idno><idno type="pmid">8855815</idno><idno type="doi">10.1210/jcem.81.10.8855815</idno><idno type="wicri:Area/PubMed/Corpus">000950</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000950</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Short-term estradiol treatment enhances pituitary-adrenal axis and sympathetic responses to psychosocial stress in healthy young men.</title><author><name sortKey="Kirschbaum, C" sort="Kirschbaum, C" uniqKey="Kirschbaum C" first="C" last="Kirschbaum">C. Kirschbaum</name><affiliation><nlm:affiliation>Center for Psychobiological, University of Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Schommer, N" sort="Schommer, N" uniqKey="Schommer N" first="N" last="Schommer">N. Schommer</name></author><author><name sortKey="Federenko, I" sort="Federenko, I" uniqKey="Federenko I" first="I" last="Federenko">I. Federenko</name></author><author><name sortKey="Gaab, J" sort="Gaab, J" uniqKey="Gaab J" first="J" last="Gaab">J. Gaab</name></author><author><name sortKey="Neumann, O" sort="Neumann, O" uniqKey="Neumann O" first="O" last="Neumann">O. Neumann</name></author><author><name sortKey="Oellers, M" sort="Oellers, M" uniqKey="Oellers M" first="M" last="Oellers">M. Oellers</name></author><author><name sortKey="Rohleder, N" sort="Rohleder, N" uniqKey="Rohleder N" first="N" last="Rohleder">N. Rohleder</name></author><author><name sortKey="Untiedt, A" sort="Untiedt, A" uniqKey="Untiedt A" first="A" last="Untiedt">A. Untiedt</name></author><author><name sortKey="Hanker, J" sort="Hanker, J" uniqKey="Hanker J" first="J" last="Hanker">J. Hanker</name></author><author><name sortKey="Pirke, K M" sort="Pirke, K M" uniqKey="Pirke K" first="K M" last="Pirke">K M Pirke</name></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D H" last="Hellhammer">D H Hellhammer</name></author></analytic><series><title level="j">The Journal of clinical endocrinology and metabolism</title><idno type="ISSN">0021-972X</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenal Glands (physiology)</term><term>Adrenocorticotropic Hormone (blood)</term><term>Adult</term><term>Estradiol (administration & dosage)</term><term>Estradiol (therapeutic use)</term><term>Heart Rate</term><term>Humans</term><term>Hydrocortisone (blood)</term><term>Kinetics</term><term>Male</term><term>Norepinephrine (blood)</term><term>Pituitary Gland (physiology)</term><term>Stress, Psychological (drug therapy)</term><term>Stress, Psychological (physiopathology)</term><term>Sympathetic Nervous System (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Estradiol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Adrenocorticotropic Hormone</term><term>Hydrocortisone</term><term>Norepinephrine</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Adrenal Glands</term><term>Pituitary Gland</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Stress, Psychological</term><term>Sympathetic Nervous System</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Estradiol</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Heart Rate</term><term>Humans</term><term>Kinetics</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Evidence from animal studies and clinical observations suggest that the activity of the pituitary-adrenal axis is under significant influence of sex steroids. The present study investigated how a short term elevation of estradiol levels affects ACTH, cortisol, norepinephrine, and heart rate responses to mental stress in healthy men. In a double blind study, 16 men received a patch delivering 0.1 mg estradiol/day transdermally, and age- and body mass index-matched control subjects received a placebo patch. Twenty-four to 48 h later, they were exposed to a brief psychosocial stressor (free speech and mental arithmetic in front of an audience). In response to the psychosocial stressor, ACTH, cortisol, norepinephrine, and heart rate were increased in both experimental groups (all P < 0.0001). However, the estradiol-treated subjects showed exaggerated peak ACTH (P < 0.001) and cortisol (P < 0.002) responses compared to the placebo group. Also, the norepinephrine area under the response curve was greater in the estradiol group (P < 0.05). Although heart rate responses differences failed to reach statistical significance, they, too, tended to be larger in the estradiol group. Neither mood ratings before or after the stressor, nor ratings of the perception of the stressor could explain the observed endocrine response differences. In conclusion, short term estradiol administration resulted in hyperresponses of the pituitary-adrenal axis and norepinephrine to psychosocial stress in healthy young men independent of psychological effects, as assessed in this study.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8855815</PMID><DateCreated><Year>1996</Year><Month>11</Month><Day>19</Day></DateCreated><DateCompleted><Year>1996</Year><Month>11</Month><Day>19</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0021-972X</ISSN><JournalIssue CitedMedium="Print"><Volume>81</Volume><Issue>10</Issue><PubDate><Year>1996</Year><Month>Oct</Month></PubDate></JournalIssue><Title>The Journal of clinical endocrinology and metabolism</Title><ISOAbbreviation>J. Clin. Endocrinol. Metab.</ISOAbbreviation></Journal><ArticleTitle>Short-term estradiol treatment enhances pituitary-adrenal axis and sympathetic responses to psychosocial stress in healthy young men.</ArticleTitle><Pagination><MedlinePgn>3639-43</MedlinePgn></Pagination><Abstract><AbstractText>Evidence from animal studies and clinical observations suggest that the activity of the pituitary-adrenal axis is under significant influence of sex steroids. The present study investigated how a short term elevation of estradiol levels affects ACTH, cortisol, norepinephrine, and heart rate responses to mental stress in healthy men. In a double blind study, 16 men received a patch delivering 0.1 mg estradiol/day transdermally, and age- and body mass index-matched control subjects received a placebo patch. Twenty-four to 48 h later, they were exposed to a brief psychosocial stressor (free speech and mental arithmetic in front of an audience). In response to the psychosocial stressor, ACTH, cortisol, norepinephrine, and heart rate were increased in both experimental groups (all P < 0.0001). However, the estradiol-treated subjects showed exaggerated peak ACTH (P < 0.001) and cortisol (P < 0.002) responses compared to the placebo group. Also, the norepinephrine area under the response curve was greater in the estradiol group (P < 0.05). Although heart rate responses differences failed to reach statistical significance, they, too, tended to be larger in the estradiol group. Neither mood ratings before or after the stressor, nor ratings of the perception of the stressor could explain the observed endocrine response differences. In conclusion, short term estradiol administration resulted in hyperresponses of the pituitary-adrenal axis and norepinephrine to psychosocial stress in healthy young men independent of psychological effects, as assessed in this study.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kirschbaum</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Center for Psychobiological, University of Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schommer</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Federenko</LastName><ForeName>I</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Gaab</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Neumann</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Oellers</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Rohleder</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Untiedt</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Hanker</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Pirke</LastName><ForeName>K M</ForeName><Initials>KM</Initials></Author><Author ValidYN="Y"><LastName>Hellhammer</LastName><ForeName>D H</ForeName><Initials>DH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Endocrinol Metab</MedlineTA><NlmUniqueID>0375362</NlmUniqueID><ISSNLinking>0021-972X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>4TI98Z838E</RegistryNumber><NameOfSubstance UI="D004958">Estradiol</NameOfSubstance></Chemical><Chemical><RegistryNumber>9002-60-2</RegistryNumber><NameOfSubstance UI="D000324">Adrenocorticotropic Hormone</NameOfSubstance></Chemical><Chemical><RegistryNumber>WI4X0X7BPJ</RegistryNumber><NameOfSubstance UI="D006854">Hydrocortisone</NameOfSubstance></Chemical><Chemical><RegistryNumber>X4W3ENH1CV</RegistryNumber><NameOfSubstance UI="D009638">Norepinephrine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>J Clin Endocrinol Metab. 1997 Mar;82(3):982</RefSource><PMID Version="1">9062517</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000311" MajorTopicYN="N">Adrenal Glands</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000324" MajorTopicYN="N">Adrenocorticotropic Hormone</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004958" MajorTopicYN="N">Estradiol</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="N">Heart Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006854" MajorTopicYN="N">Hydrocortisone</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009638" MajorTopicYN="N">Norepinephrine</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010902" MajorTopicYN="N">Pituitary Gland</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013315" MajorTopicYN="N">Stress, Psychological</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013564" MajorTopicYN="N">Sympathetic Nervous System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>10</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8855815</ArticleId><ArticleId IdType="doi">10.1210/jcem.81.10.8855815</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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