LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR
Identifieur interne : 002812 ( Istex/Corpus ); précédent : 002811; suivant : 002813LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR
Auteurs : C. R. W. Edwards ; D. Burt ; M. A. Mcintyre ; E. R. De Kloet ; P. M. Stewart ; L. Brett ; W. S. Sutanto ; C. MonderSource :
- The Lancet [ 0140-6736 ] ; 1988.
Abstract
In vitro the mineralocorticoid receptor is non-specific and does not distinguish between aldosterone and cortisol. In vivo certain tissues with this receptor are aldosterone selective (eg, kidney and parotid) whereas others with the same receptor are not (eg, hippocampus and heart). Experiments in rats showed that 11β-hydroxysteroid dehydrogenase (which converts cortisol to cortisone in man and corticosterone to 11-dehydrocorticosterone in the rat) was much more highly concentrated in aldosterone-selective tissues than in non-selective tissues. The localisation in the selective tissues was such that the enzyme could act as a paracrine or possibly an autocrine mechanism protecting the receptor from exposure to corticosterone. Autoradiographic studies showed that protection is lost when the enzyme is inhibited; 3H-corticosterone and 3H-aldosterone were bound to similar sites. These findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11β-OHSD and those in whom the enzyme has been inhibited by liquorice.
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DOI: 10.1016/S0140-6736(88)90742-8
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</title><author><name sortKey="Edwards, C R W" sort="Edwards, C R W" uniqKey="Edwards C" first="C. R. W." last="Edwards">C. R. W. Edwards</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Burt, D" sort="Burt, D" uniqKey="Burt D" first="D." last="Burt">D. Burt</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Mcintyre, M A" sort="Mcintyre, M A" uniqKey="Mcintyre M" first="M. A." last="Mcintyre">M. A. Mcintyre</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="De Kloet, E R" sort="De Kloet, E R" uniqKey="De Kloet E" first="E. R." last="De Kloet">E. R. De Kloet</name><affiliation><mods:affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Stewart, P M" sort="Stewart, P M" uniqKey="Stewart P" first="P. M." last="Stewart">P. M. Stewart</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Brett, L" sort="Brett, L" uniqKey="Brett L" first="L." last="Brett">L. Brett</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Sutanto, W S" sort="Sutanto, W S" uniqKey="Sutanto W" first="W. S." last="Sutanto">W. S. Sutanto</name><affiliation><mods:affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Monder, C" sort="Monder, C" uniqKey="Monder C" first="C." last="Monder">C. Monder</name><affiliation><mods:affiliation>Population Council, New York, NY 10021, U.S.A.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A151C90D4994033ED57D24D6F34D76D507D33FEB</idno><date when="1988" year="1988">1988</date><idno type="doi">10.1016/S0140-6736(88)90742-8</idno><idno type="url">https://api.istex.fr/document/A151C90D4994033ED57D24D6F34D76D507D33FEB/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002812</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</title><author><name sortKey="Edwards, C R W" sort="Edwards, C R W" uniqKey="Edwards C" first="C. R. W." last="Edwards">C. R. W. Edwards</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Burt, D" sort="Burt, D" uniqKey="Burt D" first="D." last="Burt">D. Burt</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Mcintyre, M A" sort="Mcintyre, M A" uniqKey="Mcintyre M" first="M. A." last="Mcintyre">M. A. Mcintyre</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="De Kloet, E R" sort="De Kloet, E R" uniqKey="De Kloet E" first="E. R." last="De Kloet">E. R. De Kloet</name><affiliation><mods:affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Stewart, P M" sort="Stewart, P M" uniqKey="Stewart P" first="P. M." last="Stewart">P. M. Stewart</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Brett, L" sort="Brett, L" uniqKey="Brett L" first="L." last="Brett">L. Brett</name><affiliation><mods:affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</mods:affiliation></affiliation></author><author><name sortKey="Sutanto, W S" sort="Sutanto, W S" uniqKey="Sutanto W" first="W. S." last="Sutanto">W. S. Sutanto</name><affiliation><mods:affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Monder, C" sort="Monder, C" uniqKey="Monder C" first="C." last="Monder">C. Monder</name><affiliation><mods:affiliation>Population Council, New York, NY 10021, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The Lancet</title><title level="j" type="abbrev">LANCET</title><idno type="ISSN">0140-6736</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988">1988</date><biblScope unit="volume">332</biblScope><biblScope unit="issue">8618</biblScope><biblScope unit="page" from="986">986</biblScope><biblScope unit="page" to="989">989</biblScope></imprint><idno type="ISSN">0140-6736</idno></series><idno type="istex">A151C90D4994033ED57D24D6F34D76D507D33FEB</idno><idno type="DOI">10.1016/S0140-6736(88)90742-8</idno><idno type="PII">S0140-6736(88)90742-8</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0140-6736</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In vitro the mineralocorticoid receptor is non-specific and does not distinguish between aldosterone and cortisol. In vivo certain tissues with this receptor are aldosterone selective (eg, kidney and parotid) whereas others with the same receptor are not (eg, hippocampus and heart). Experiments in rats showed that 11β-hydroxysteroid dehydrogenase (which converts cortisol to cortisone in man and corticosterone to 11-dehydrocorticosterone in the rat) was much more highly concentrated in aldosterone-selective tissues than in non-selective tissues. The localisation in the selective tissues was such that the enzyme could act as a paracrine or possibly an autocrine mechanism protecting the receptor from exposure to corticosterone. Autoradiographic studies showed that protection is lost when the enzyme is inhibited; 3H-corticosterone and 3H-aldosterone were bound to similar sites. These findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11β-OHSD and those in whom the enzyme has been inhibited by liquorice.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>C.R.W. Edwards</name><affiliations><json:string>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</json:string></affiliations></json:item><json:item><name>D. Burt</name><affiliations><json:string>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</json:string></affiliations></json:item><json:item><name>M.A. Mcintyre</name><affiliations><json:string>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</json:string></affiliations></json:item><json:item><name>E.R. De Kloet</name><affiliations><json:string>Rudolf Magnus Institute, Utrecht;, The Netherlands</json:string></affiliations></json:item><json:item><name>P.M. Stewart</name><affiliations><json:string>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</json:string></affiliations></json:item><json:item><name>L. Brett</name><affiliations><json:string>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</json:string></affiliations></json:item><json:item><name>W.S. Sutanto</name><affiliations><json:string>Rudolf Magnus Institute, Utrecht;, The Netherlands</json:string></affiliations></json:item><json:item><name>C. Monder</name><affiliations><json:string>Population Council, New York, NY 10021, U.S.A.</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>In vitro the mineralocorticoid receptor is non-specific and does not distinguish between aldosterone and cortisol. In vivo certain tissues with this receptor are aldosterone selective (eg, kidney and parotid) whereas others with the same receptor are not (eg, hippocampus and heart). Experiments in rats showed that 11β-hydroxysteroid dehydrogenase (which converts cortisol to cortisone in man and corticosterone to 11-dehydrocorticosterone in the rat) was much more highly concentrated in aldosterone-selective tissues than in non-selective tissues. The localisation in the selective tissues was such that the enzyme could act as a paracrine or possibly an autocrine mechanism protecting the receptor from exposure to corticosterone. Autoradiographic studies showed that protection is lost when the enzyme is inhibited; 3H-corticosterone and 3H-aldosterone were bound to similar sites. These findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11β-OHSD and those in whom the enzyme has been inhibited by liquorice.</abstract><qualityIndicators><score>5.18</score><pdfVersion>1.2</pdfVersion><pdfPageSize>622 x 939 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1091</abstractCharCount><pdfWordCount>3356</pdfWordCount><pdfCharCount>21877</pdfCharCount><pdfPageCount>4</pdfPageCount><abstractWordCount>152</abstractWordCount></qualityIndicators><title>LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</title><pii><json:string>S0140-6736(88)90742-8</json:string></pii><genre><json:string>research-article</json:string></genre><serie><pages><last>87</last><first>86</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Adrenal 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level="a">LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1988</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</title><author><persName><forename type="first">C.R.W.</forename><surname>Edwards</surname></persName><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation></author><author><persName><forename type="first">D.</forename><surname>Burt</surname></persName><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation></author><author><persName><forename type="first">M.A.</forename><surname>Mcintyre</surname></persName><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation></author><author><persName><forename type="first">E.R.</forename><surname>De Kloet</surname></persName><affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</affiliation></author><author><persName><forename type="first">P.M.</forename><surname>Stewart</surname></persName><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation></author><author><persName><forename type="first">L.</forename><surname>Brett</surname></persName><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation></author><author><persName><forename type="first">W.S.</forename><surname>Sutanto</surname></persName><affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</affiliation></author><author><persName><forename type="first">C.</forename><surname>Monder</surname></persName><affiliation>Population Council, New York, NY 10021, U.S.A.</affiliation></author></analytic><monogr><title level="j">The Lancet</title><title level="j" type="abbrev">LANCET</title><idno type="pISSN">0140-6736</idno><idno type="PII">S0140-6736(00)X7502-2</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988"></date><biblScope unit="volume">332</biblScope><biblScope unit="issue">8618</biblScope><biblScope unit="page" from="986">986</biblScope><biblScope unit="page" to="989">989</biblScope></imprint></monogr><idno type="istex">A151C90D4994033ED57D24D6F34D76D507D33FEB</idno><idno type="DOI">10.1016/S0140-6736(88)90742-8</idno><idno type="PII">S0140-6736(88)90742-8</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In vitro the mineralocorticoid receptor is non-specific and does not distinguish between aldosterone and cortisol. In vivo certain tissues with this receptor are aldosterone selective (eg, kidney and parotid) whereas others with the same receptor are not (eg, hippocampus and heart). Experiments in rats showed that 11β-hydroxysteroid dehydrogenase (which converts cortisol to cortisone in man and corticosterone to 11-dehydrocorticosterone in the rat) was much more highly concentrated in aldosterone-selective tissues than in non-selective tissues. The localisation in the selective tissues was such that the enzyme could act as a paracrine or possibly an autocrine mechanism protecting the receptor from exposure to corticosterone. Autoradiographic studies showed that protection is lost when the enzyme is inhibited; 3H-corticosterone and 3H-aldosterone were bound to similar sites. These findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11β-OHSD and those in whom the enzyme has been inhibited by liquorice.</p></abstract></profileDesc><revisionDesc><change when="1988">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>LANCET</jid><aid>88907428</aid><ce:pii>S0140-6736(88)90742-8</ce:pii><ce:doi>10.1016/S0140-6736(88)90742-8</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright></item-info><head><ce:title>LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</ce:title><ce:author-group><ce:author><ce:given-name>C.R.W.</ce:given-name><ce:surname>Edwards</ce:surname><ce:cross-ref refid="ART3-AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>D.</ce:given-name><ce:surname>Burt</ce:surname><ce:cross-ref refid="ART3-AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>M.A.</ce:given-name><ce:surname>Mcintyre</ce:surname><ce:cross-ref refid="ART3-AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>E.R.</ce:given-name><ce:surname>De Kloet</ce:surname><ce:cross-ref refid="ART3-AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.M.</ce:given-name><ce:surname>Stewart</ce:surname><ce:cross-ref refid="ART3-AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>L.</ce:given-name><ce:surname>Brett</ce:surname><ce:cross-ref refid="ART3-AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>W.S.</ce:given-name><ce:surname>Sutanto</ce:surname><ce:cross-ref refid="ART3-AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>C.</ce:given-name><ce:surname>Monder</ce:surname><ce:cross-ref refid="ART3-AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="ART3-AFF1"><ce:label>a</ce:label><ce:textfn>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</ce:textfn></ce:affiliation><ce:affiliation id="ART3-AFF2"><ce:label>b</ce:label><ce:textfn>Rudolf Magnus Institute, Utrecht;, The Netherlands</ce:textfn></ce:affiliation><ce:affiliation id="ART3-AFF3"><ce:label>c</ce:label><ce:textfn>Population Council, New York, NY 10021, U.S.A.</ce:textfn></ce:affiliation></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>In vitro the mineralocorticoid receptor is non-specific and does not distinguish between aldosterone and cortisol. In vivo certain tissues with this receptor are aldosterone selective (eg, kidney and parotid) whereas others with the same receptor are not (eg, hippocampus and heart). Experiments in rats showed that 11β-hydroxysteroid dehydrogenase (which converts cortisol to cortisone in man and corticosterone to 11-dehydrocorticosterone in the rat) was much more highly concentrated in aldosterone-selective tissues than in non-selective tissues. The localisation in the selective tissues was such that the enzyme could act as a paracrine or possibly an autocrine mechanism protecting the receptor from exposure to corticosterone. Autoradiographic studies showed that protection is lost when the enzyme is inhibited; <ce:sup>3</ce:sup>H-corticosterone and <ce:sup>3</ce:sup>H-aldosterone were bound to similar sites. These findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11β-OHSD and those in whom the enzyme has been inhibited by liquorice.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR</title></titleInfo><name type="personal"><namePart type="given">C.R.W.</namePart><namePart type="family">Edwards</namePart><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Burt</namePart><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.A.</namePart><namePart type="family">Mcintyre</namePart><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.R.</namePart><namePart type="family">De Kloet</namePart><affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.M.</namePart><namePart type="family">Stewart</namePart><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Brett</namePart><affiliation>Departments of Medicine and Pathology, Western General Hospital, Edinburgh EH4 2XU;, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.S.</namePart><namePart type="family">Sutanto</namePart><affiliation>Rudolf Magnus Institute, Utrecht;, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Monder</namePart><affiliation>Population Council, New York, NY 10021, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1988</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">In vitro the mineralocorticoid receptor is non-specific and does not distinguish between aldosterone and cortisol. In vivo certain tissues with this receptor are aldosterone selective (eg, kidney and parotid) whereas others with the same receptor are not (eg, hippocampus and heart). Experiments in rats showed that 11β-hydroxysteroid dehydrogenase (which converts cortisol to cortisone in man and corticosterone to 11-dehydrocorticosterone in the rat) was much more highly concentrated in aldosterone-selective tissues than in non-selective tissues. The localisation in the selective tissues was such that the enzyme could act as a paracrine or possibly an autocrine mechanism protecting the receptor from exposure to corticosterone. Autoradiographic studies showed that protection is lost when the enzyme is inhibited; 3H-corticosterone and 3H-aldosterone were bound to similar sites. These findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11β-OHSD and those in whom the enzyme has been inhibited by liquorice.</abstract><relatedItem type="host"><titleInfo><title>The Lancet</title></titleInfo><titleInfo type="abbreviated"><title>LANCET</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19881029</dateIssued></originInfo><identifier type="ISSN">0140-6736</identifier><identifier type="PII">S0140-6736(00)X7502-2</identifier><part><date>19881029</date><detail type="issue"><title>Originally published as Volume 2, Issue 8618</title></detail><detail type="volume"><number>332</number><caption>vol.</caption></detail><detail type="issue"><number>8618</number><caption>no.</caption></detail><extent unit="issue pages"><start>979</start><end>1038</end></extent><extent unit="pages"><start>986</start><end>989</end></extent></part></relatedItem><identifier type="istex">A151C90D4994033ED57D24D6F34D76D507D33FEB</identifier><identifier type="DOI">10.1016/S0140-6736(88)90742-8</identifier><identifier type="PII">S0140-6736(88)90742-8</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/A151C90D4994033ED57D24D6F34D76D507D33FEB/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">MEDICINE, GENERAL & INTERNAL</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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