Aldosterone induces angiotensin-converting-enzyme gene expression in cultured neonatal rat cardiocytes
The cardiac renin-angiotensin-aldosterone system is activated in failing hearts in proportion to the severity of the disease. We hypothesized that a positive feedback mechanism might exist within this system and contribute to the progression of the heart failure. Methods and Results-- To test this h...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2001-07, Vol.104 (2), p.137-139 |
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| creator | HARADA, Eisaku YOSHIMURA, Michihiro NAKAMURA, Shota KUWAHARA, Koichiro SAITO, Yoshihiko NAKAO, Kazuwa OGAWA, Hisao YASUE, Hirofumi NAKAGAWA, Osamu NAKAGAWA, Masayo HARADA, Masaki MIZUNO, Yuji NAKAYAMA, Masafumi SHIMASAKI, Yukio ITO, Teruhiko |
| description | The cardiac renin-angiotensin-aldosterone system is activated in failing hearts in proportion to the severity of the disease. We hypothesized that a positive feedback mechanism might exist within this system and contribute to the progression of the heart failure. Methods and Results-- To test this hypothesis, we examined whether angiotensin II or aldosterone induces the expression of angiotensin-converting-enzyme (ACE) mRNA in cultured neonatal rat ventricular cardiocytes. Expression of ACE mRNA was detected and quantified using real-time reverse transcription-polymerase chain reaction. Exposure to angiotensin II (10(-5) mol/L) for 24 hours had no significant effect on the expression of ACE mRNA (0.7+/-0.5-fold versus control, P=NS), but similar treatment with aldosterone (10(-5) mol/L) induced a 23.3+/-7.9-fold increase (P |
| doi_str_mv | 10.1161/01.cir.104.2.137 |
| format | Article |
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Aldosterone upregulates ACE mRNA expression, which is blocked by spironolactone in neonatal rat cardiocytes. Thus, spironolactone may suppress the progression of heart failure by blocking the effects of aldosterone and angiotensin II.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.104.2.137</identifier><identifier>PMID: 11447075</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aldosterone - pharmacology ; Angiotensin II - antagonists & inhibitors ; Angiotensin II - pharmacology ; Animals ; Animals, Newborn ; Biological and medical sciences ; Calibration ; Cells, Cultured ; Dose-Response Relationship, Drug ; Fundamental and applied biological sciences. Psychology ; Gene Expression - drug effects ; Heart ; Heart Ventricles - cytology ; Heart Ventricles - drug effects ; Heart Ventricles - metabolism ; Lung - chemistry ; Lung - metabolism ; Mineralocorticoid Receptor Antagonists - pharmacology ; Myocardium - cytology ; Myocardium - metabolism ; Peptidyl-Dipeptidase A - biosynthesis ; Peptidyl-Dipeptidase A - genetics ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; RNA, Messenger - biosynthesis ; Spironolactone - pharmacology ; Up-Regulation - drug effects ; Vertebrates: cardiovascular system</subject><ispartof>Circulation (New York, N.Y.), 2001-07, Vol.104 (2), p.137-139</ispartof><rights>2001 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jul 10, 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c547t-3e91267dc6f05f134dce70836a4aec5937c8775e4090546012543e38b8567683</citedby><cites>FETCH-LOGICAL-c547t-3e91267dc6f05f134dce70836a4aec5937c8775e4090546012543e38b8567683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27902,27903</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1052049$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11447075$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HARADA, Eisaku</creatorcontrib><creatorcontrib>YOSHIMURA, Michihiro</creatorcontrib><creatorcontrib>NAKAMURA, Shota</creatorcontrib><creatorcontrib>KUWAHARA, Koichiro</creatorcontrib><creatorcontrib>SAITO, Yoshihiko</creatorcontrib><creatorcontrib>NAKAO, Kazuwa</creatorcontrib><creatorcontrib>OGAWA, Hisao</creatorcontrib><creatorcontrib>YASUE, Hirofumi</creatorcontrib><creatorcontrib>NAKAGAWA, Osamu</creatorcontrib><creatorcontrib>NAKAGAWA, Masayo</creatorcontrib><creatorcontrib>HARADA, Masaki</creatorcontrib><creatorcontrib>MIZUNO, Yuji</creatorcontrib><creatorcontrib>NAKAYAMA, Masafumi</creatorcontrib><creatorcontrib>SHIMASAKI, Yukio</creatorcontrib><creatorcontrib>ITO, Teruhiko</creatorcontrib><title>Aldosterone induces angiotensin-converting-enzyme gene expression in cultured neonatal rat cardiocytes</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>The cardiac renin-angiotensin-aldosterone system is activated in failing hearts in proportion to the severity of the disease. We hypothesized that a positive feedback mechanism might exist within this system and contribute to the progression of the heart failure. Methods and Results-- To test this hypothesis, we examined whether angiotensin II or aldosterone induces the expression of angiotensin-converting-enzyme (ACE) mRNA in cultured neonatal rat ventricular cardiocytes. Expression of ACE mRNA was detected and quantified using real-time reverse transcription-polymerase chain reaction. Exposure to angiotensin II (10(-5) mol/L) for 24 hours had no significant effect on the expression of ACE mRNA (0.7+/-0.5-fold versus control, P=NS), but similar treatment with aldosterone (10(-5) mol/L) induced a 23.3+/-7.9-fold increase (P<0.01) in ACE mRNA expression. The effect of aldosterone was both time- (maximal effect, 24 hours) and dose-dependent (EC(50), 4x10(-7) mol/L), and it was significantly (P<0.01) inhibited by spironolactone, a specific mineralocorticoid receptor antagonist.
Aldosterone upregulates ACE mRNA expression, which is blocked by spironolactone in neonatal rat cardiocytes. Thus, spironolactone may suppress the progression of heart failure by blocking the effects of aldosterone and angiotensin II.</description><subject>Aldosterone - pharmacology</subject><subject>Angiotensin II - antagonists & inhibitors</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Calibration</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - drug effects</subject><subject>Heart</subject><subject>Heart Ventricles - cytology</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - metabolism</subject><subject>Lung - chemistry</subject><subject>Lung - metabolism</subject><subject>Mineralocorticoid Receptor Antagonists - pharmacology</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Peptidyl-Dipeptidase A - biosynthesis</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Rats</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Spironolactone - pharmacology</subject><subject>Up-Regulation - drug effects</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM9rFDEcxUNR7LZ670kGKd5mzDc_J8eyWC0UBOk9pJnvLCmzyZpkxPWvN9IFpafHg897PB4hV0AHAAWfKAw-5AGoGNgAXJ-RDUgmeiG5eUU2lFLTa87YObko5alZxbV8Q84BhNBUyw2Zb5YplYo5RexCnFaPpXNxF1LFWELsfYo_MdcQdz3G38c9djtsKP46ZCwlpNhSnV-XumacuogpuuqWLrvaeZenkPyxYnlLXs9uKfjupJfk4fbzw_Zrf__ty9325r73UujaczTAlJ68mqmcgYvJo6YjV0449NJw7UetJQpqqBSKApOCIx8fR6m0Gvkl-fhce8jpx4ql2n0oHpfFtWFrsZqa0fBRNvDDC_AprTm2aZYB05yDUQ2iz5DPqZSMsz3ksHf5aIHav_9bCnZ7971ZYZlt_7fI-1Pv-rjH6V_gdHgDrk-AK94tc3bRh_JfsWRUGP4HC4KODQ</recordid><startdate>20010710</startdate><enddate>20010710</enddate><creator>HARADA, Eisaku</creator><creator>YOSHIMURA, Michihiro</creator><creator>NAKAMURA, Shota</creator><creator>KUWAHARA, Koichiro</creator><creator>SAITO, Yoshihiko</creator><creator>NAKAO, Kazuwa</creator><creator>OGAWA, Hisao</creator><creator>YASUE, Hirofumi</creator><creator>NAKAGAWA, Osamu</creator><creator>NAKAGAWA, Masayo</creator><creator>HARADA, Masaki</creator><creator>MIZUNO, Yuji</creator><creator>NAKAYAMA, Masafumi</creator><creator>SHIMASAKI, Yukio</creator><creator>ITO, Teruhiko</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20010710</creationdate><title>Aldosterone induces angiotensin-converting-enzyme gene expression in cultured neonatal rat cardiocytes</title><author>HARADA, Eisaku ; YOSHIMURA, Michihiro ; NAKAMURA, Shota ; KUWAHARA, Koichiro ; SAITO, Yoshihiko ; NAKAO, Kazuwa ; OGAWA, Hisao ; YASUE, Hirofumi ; NAKAGAWA, Osamu ; NAKAGAWA, Masayo ; HARADA, Masaki ; MIZUNO, Yuji ; NAKAYAMA, Masafumi ; SHIMASAKI, Yukio ; ITO, Teruhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c547t-3e91267dc6f05f134dce70836a4aec5937c8775e4090546012543e38b8567683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Aldosterone - pharmacology</topic><topic>Angiotensin II - antagonists & inhibitors</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biological and medical sciences</topic><topic>Calibration</topic><topic>Cells, Cultured</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression - drug effects</topic><topic>Heart</topic><topic>Heart Ventricles - cytology</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - metabolism</topic><topic>Lung - chemistry</topic><topic>Lung - metabolism</topic><topic>Mineralocorticoid Receptor Antagonists - pharmacology</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Peptidyl-Dipeptidase A - biosynthesis</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Rats</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Spironolactone - pharmacology</topic><topic>Up-Regulation - drug effects</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HARADA, Eisaku</creatorcontrib><creatorcontrib>YOSHIMURA, Michihiro</creatorcontrib><creatorcontrib>NAKAMURA, Shota</creatorcontrib><creatorcontrib>KUWAHARA, Koichiro</creatorcontrib><creatorcontrib>SAITO, Yoshihiko</creatorcontrib><creatorcontrib>NAKAO, Kazuwa</creatorcontrib><creatorcontrib>OGAWA, Hisao</creatorcontrib><creatorcontrib>YASUE, Hirofumi</creatorcontrib><creatorcontrib>NAKAGAWA, Osamu</creatorcontrib><creatorcontrib>NAKAGAWA, Masayo</creatorcontrib><creatorcontrib>HARADA, Masaki</creatorcontrib><creatorcontrib>MIZUNO, Yuji</creatorcontrib><creatorcontrib>NAKAYAMA, Masafumi</creatorcontrib><creatorcontrib>SHIMASAKI, Yukio</creatorcontrib><creatorcontrib>ITO, Teruhiko</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 Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HARADA, Eisaku</au><au>YOSHIMURA, Michihiro</au><au>NAKAMURA, Shota</au><au>KUWAHARA, Koichiro</au><au>SAITO, Yoshihiko</au><au>NAKAO, Kazuwa</au><au>OGAWA, Hisao</au><au>YASUE, Hirofumi</au><au>NAKAGAWA, Osamu</au><au>NAKAGAWA, Masayo</au><au>HARADA, Masaki</au><au>MIZUNO, Yuji</au><au>NAKAYAMA, Masafumi</au><au>SHIMASAKI, Yukio</au><au>ITO, Teruhiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aldosterone induces angiotensin-converting-enzyme gene expression in cultured neonatal rat cardiocytes</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2001-07-10</date><risdate>2001</risdate><volume>104</volume><issue>2</issue><spage>137</spage><epage>139</epage><pages>137-139</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>The cardiac renin-angiotensin-aldosterone system is activated in failing hearts in proportion to the severity of the disease. We hypothesized that a positive feedback mechanism might exist within this system and contribute to the progression of the heart failure. Methods and Results-- To test this hypothesis, we examined whether angiotensin II or aldosterone induces the expression of angiotensin-converting-enzyme (ACE) mRNA in cultured neonatal rat ventricular cardiocytes. Expression of ACE mRNA was detected and quantified using real-time reverse transcription-polymerase chain reaction. Exposure to angiotensin II (10(-5) mol/L) for 24 hours had no significant effect on the expression of ACE mRNA (0.7+/-0.5-fold versus control, P=NS), but similar treatment with aldosterone (10(-5) mol/L) induced a 23.3+/-7.9-fold increase (P<0.01) in ACE mRNA expression. The effect of aldosterone was both time- (maximal effect, 24 hours) and dose-dependent (EC(50), 4x10(-7) mol/L), and it was significantly (P<0.01) inhibited by spironolactone, a specific mineralocorticoid receptor antagonist.
Aldosterone upregulates ACE mRNA expression, which is blocked by spironolactone in neonatal rat cardiocytes. Thus, spironolactone may suppress the progression of heart failure by blocking the effects of aldosterone and angiotensin II.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11447075</pmid><doi>10.1161/01.cir.104.2.137</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aldosterone - pharmacology Angiotensin II - antagonists & inhibitors Angiotensin II - pharmacology Animals Animals, Newborn Biological and medical sciences Calibration Cells, Cultured Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology Gene Expression - drug effects Heart Heart Ventricles - cytology Heart Ventricles - drug effects Heart Ventricles - metabolism Lung - chemistry Lung - metabolism Mineralocorticoid Receptor Antagonists - pharmacology Myocardium - cytology Myocardium - metabolism Peptidyl-Dipeptidase A - biosynthesis Peptidyl-Dipeptidase A - genetics Rats Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis RNA, Messenger - biosynthesis Spironolactone - pharmacology Up-Regulation - drug effects Vertebrates: cardiovascular system |
| title | Aldosterone induces angiotensin-converting-enzyme gene expression in cultured neonatal rat cardiocytes |
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