Magnesium supplementation prevents angiotensin II-induced myocardial damage and CTGF overexpression
Magnesium deficiency promotes vasoconstriction and myocardial damage. Recent studies provide evidence that Ang II mobilizes intracellular Mg through AT1 receptor-mediated pathways. We tested the hypothesis of whether magnesium supplementation prevents Ang II-induced myocardial damage and induction o...
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| Veröffentlicht in: | Journal of hypertension 2005-02, Vol.23 (2), p.375-380 |
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| container_title | Journal of hypertension |
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| creator | Finckenberg, Piet Merasto, Saara Louhelainen, Marjut Lindgren, Leena Vapaatalo, Heikki Müller, Dominik N Luft, Friedrich C Mervaala, Eero M A |
| description | Magnesium deficiency promotes vasoconstriction and myocardial damage. Recent studies provide evidence that Ang II mobilizes intracellular Mg through AT1 receptor-mediated pathways. We tested the hypothesis of whether magnesium supplementation prevents Ang II-induced myocardial damage and induction of the profibrotic connective tissue growth factor (CTGF).
Four-week-old double transgenic rats harboring human renin and angiotensinogen genes (dTGR) were given dietary magnesium supplementation (0.6%) for 3 weeks. Control dTGR and normotensive Sprague-Dawley (SD) rats received normal diet (Mg 0.2%). Histopathological, immunohistochemical and mRNA analysis were used to detect the treatment-related effects of dietary magnesium in dTGR.
Magnesium (Mg) supplementation decreased blood pressure, ameliorated cardiac hypertrophy, protected against the development of Ang II-induced myocardial damage and increased serum ionized Mg2+ concentration (all variables P < 0.05). There was no difference in serum ionized Mg2+ concentration between dTGR and SD rats. Myocardial connective tissue growth factor (CTGF) mRNA and protein expressions were increased by 300% in dTGR (P < 0.05), especially in areas with myocardial infarctions and vascular inflammation. Magnesium supplementation prevented Ang II-induced myocardial CTGF overexpression (P < 0.05). Magnesium supplementation also improved the therapeutic effects of the calcineurin inhibitor tacrolimus, which produced marked hypomagnesemia when given as monotherapy.
Our findings suggest a salutary effect for magnesium supplementation in the treatment of Ang II-induced myocardial complications. |
| doi_str_mv | 10.1097/00004872-200502000-00020 |
| format | Article |
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Four-week-old double transgenic rats harboring human renin and angiotensinogen genes (dTGR) were given dietary magnesium supplementation (0.6%) for 3 weeks. Control dTGR and normotensive Sprague-Dawley (SD) rats received normal diet (Mg 0.2%). Histopathological, immunohistochemical and mRNA analysis were used to detect the treatment-related effects of dietary magnesium in dTGR.
Magnesium (Mg) supplementation decreased blood pressure, ameliorated cardiac hypertrophy, protected against the development of Ang II-induced myocardial damage and increased serum ionized Mg2+ concentration (all variables P < 0.05). There was no difference in serum ionized Mg2+ concentration between dTGR and SD rats. Myocardial connective tissue growth factor (CTGF) mRNA and protein expressions were increased by 300% in dTGR (P < 0.05), especially in areas with myocardial infarctions and vascular inflammation. Magnesium supplementation prevented Ang II-induced myocardial CTGF overexpression (P < 0.05). Magnesium supplementation also improved the therapeutic effects of the calcineurin inhibitor tacrolimus, which produced marked hypomagnesemia when given as monotherapy.
Our findings suggest a salutary effect for magnesium supplementation in the treatment of Ang II-induced myocardial complications.</description><identifier>ISSN: 0263-6352</identifier><identifier>DOI: 10.1097/00004872-200502000-00020</identifier><identifier>PMID: 15662226</identifier><language>eng</language><publisher>England</publisher><subject>Angiotensin II - pharmacology ; Angiotensinogen - genetics ; Animals ; Animals, Genetically Modified ; Blood Pressure - drug effects ; Cardiomegaly - therapy ; Connective Tissue Growth Factor ; Dietary Supplements ; Fibrosis - prevention & control ; Humans ; Immediate-Early Proteins - drug effects ; Immediate-Early Proteins - metabolism ; Immunosuppressive Agents - therapeutic use ; Intercellular Signaling Peptides and Proteins - metabolism ; Magnesium - administration & dosage ; Magnesium - blood ; Magnesium - metabolism ; Male ; Myocardium - pathology ; Rats ; Rats, Sprague-Dawley ; Renin - genetics ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Tacrolimus - therapeutic use</subject><ispartof>Journal of hypertension, 2005-02, Vol.23 (2), p.375-380</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15662226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Finckenberg, Piet</creatorcontrib><creatorcontrib>Merasto, Saara</creatorcontrib><creatorcontrib>Louhelainen, Marjut</creatorcontrib><creatorcontrib>Lindgren, Leena</creatorcontrib><creatorcontrib>Vapaatalo, Heikki</creatorcontrib><creatorcontrib>Müller, Dominik N</creatorcontrib><creatorcontrib>Luft, Friedrich C</creatorcontrib><creatorcontrib>Mervaala, Eero M A</creatorcontrib><title>Magnesium supplementation prevents angiotensin II-induced myocardial damage and CTGF overexpression</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>Magnesium deficiency promotes vasoconstriction and myocardial damage. Recent studies provide evidence that Ang II mobilizes intracellular Mg through AT1 receptor-mediated pathways. We tested the hypothesis of whether magnesium supplementation prevents Ang II-induced myocardial damage and induction of the profibrotic connective tissue growth factor (CTGF).
Four-week-old double transgenic rats harboring human renin and angiotensinogen genes (dTGR) were given dietary magnesium supplementation (0.6%) for 3 weeks. Control dTGR and normotensive Sprague-Dawley (SD) rats received normal diet (Mg 0.2%). Histopathological, immunohistochemical and mRNA analysis were used to detect the treatment-related effects of dietary magnesium in dTGR.
Magnesium (Mg) supplementation decreased blood pressure, ameliorated cardiac hypertrophy, protected against the development of Ang II-induced myocardial damage and increased serum ionized Mg2+ concentration (all variables P < 0.05). There was no difference in serum ionized Mg2+ concentration between dTGR and SD rats. Myocardial connective tissue growth factor (CTGF) mRNA and protein expressions were increased by 300% in dTGR (P < 0.05), especially in areas with myocardial infarctions and vascular inflammation. Magnesium supplementation prevented Ang II-induced myocardial CTGF overexpression (P < 0.05). Magnesium supplementation also improved the therapeutic effects of the calcineurin inhibitor tacrolimus, which produced marked hypomagnesemia when given as monotherapy.
Our findings suggest a salutary effect for magnesium supplementation in the treatment of Ang II-induced myocardial complications.</description><subject>Angiotensin II - pharmacology</subject><subject>Angiotensinogen - genetics</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiomegaly - therapy</subject><subject>Connective Tissue Growth Factor</subject><subject>Dietary Supplements</subject><subject>Fibrosis - prevention & control</subject><subject>Humans</subject><subject>Immediate-Early Proteins - drug effects</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Immunosuppressive Agents - therapeutic use</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Magnesium - administration & dosage</subject><subject>Magnesium - blood</subject><subject>Magnesium - metabolism</subject><subject>Male</subject><subject>Myocardium - pathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renin - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Tacrolimus - therapeutic use</subject><issn>0263-6352</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kMFOwzAMhnMAsTF4BZQTt4KTtGl7RBMbk4a4jHPlJu4U1KalaSf29kRi_JJt2fr0HcwYF_AkoMyfISYtcplIgAxigySWhCu2BKlVolUmF-w2hK94Lspc3bCFyLSWUuolM-949BTc3PEwD0NLHfkJJ9d7Pox0ikvg6I-un8gH5_lulzhvZ0OWd-fe4Ggdttxih0eKoOXrw3bD-xON9BMFIUTTHbtusA10f5kr9rl5Pazfkv3Hdrd-2SeDUOWU1Kh0LmujRK1NXoCSSI1Om1LWaMiAKBQAplRgLUyNRVNmAI2yqbBkCKVascc_7zD23zOFqepcMNS26KmfQ6VzpWNUBB8u4Fx3ZKthdB2O5-r_LeoXJodmqw</recordid><startdate>200502</startdate><enddate>200502</enddate><creator>Finckenberg, Piet</creator><creator>Merasto, Saara</creator><creator>Louhelainen, Marjut</creator><creator>Lindgren, Leena</creator><creator>Vapaatalo, Heikki</creator><creator>Müller, Dominik N</creator><creator>Luft, Friedrich C</creator><creator>Mervaala, Eero M A</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200502</creationdate><title>Magnesium supplementation prevents angiotensin II-induced myocardial damage and CTGF overexpression</title><author>Finckenberg, Piet ; Merasto, Saara ; Louhelainen, Marjut ; Lindgren, Leena ; Vapaatalo, Heikki ; Müller, Dominik N ; Luft, Friedrich C ; Mervaala, Eero M A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p139t-ba3672bc31b6c78032aef64f92bacec018300a4e8ab1cba8f9500f3d41decea23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Angiotensinogen - genetics</topic><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiomegaly - therapy</topic><topic>Connective Tissue Growth Factor</topic><topic>Dietary Supplements</topic><topic>Fibrosis - prevention & control</topic><topic>Humans</topic><topic>Immediate-Early Proteins - drug effects</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Immunosuppressive Agents - therapeutic use</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Magnesium - administration & dosage</topic><topic>Magnesium - blood</topic><topic>Magnesium - metabolism</topic><topic>Male</topic><topic>Myocardium - pathology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renin - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Tacrolimus - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Finckenberg, Piet</creatorcontrib><creatorcontrib>Merasto, Saara</creatorcontrib><creatorcontrib>Louhelainen, Marjut</creatorcontrib><creatorcontrib>Lindgren, Leena</creatorcontrib><creatorcontrib>Vapaatalo, Heikki</creatorcontrib><creatorcontrib>Müller, Dominik N</creatorcontrib><creatorcontrib>Luft, Friedrich C</creatorcontrib><creatorcontrib>Mervaala, Eero M A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Finckenberg, Piet</au><au>Merasto, Saara</au><au>Louhelainen, Marjut</au><au>Lindgren, Leena</au><au>Vapaatalo, Heikki</au><au>Müller, Dominik N</au><au>Luft, Friedrich C</au><au>Mervaala, Eero M A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Magnesium supplementation prevents angiotensin II-induced myocardial damage and CTGF overexpression</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2005-02</date><risdate>2005</risdate><volume>23</volume><issue>2</issue><spage>375</spage><epage>380</epage><pages>375-380</pages><issn>0263-6352</issn><abstract>Magnesium deficiency promotes vasoconstriction and myocardial damage. Recent studies provide evidence that Ang II mobilizes intracellular Mg through AT1 receptor-mediated pathways. We tested the hypothesis of whether magnesium supplementation prevents Ang II-induced myocardial damage and induction of the profibrotic connective tissue growth factor (CTGF).
Four-week-old double transgenic rats harboring human renin and angiotensinogen genes (dTGR) were given dietary magnesium supplementation (0.6%) for 3 weeks. Control dTGR and normotensive Sprague-Dawley (SD) rats received normal diet (Mg 0.2%). Histopathological, immunohistochemical and mRNA analysis were used to detect the treatment-related effects of dietary magnesium in dTGR.
Magnesium (Mg) supplementation decreased blood pressure, ameliorated cardiac hypertrophy, protected against the development of Ang II-induced myocardial damage and increased serum ionized Mg2+ concentration (all variables P < 0.05). There was no difference in serum ionized Mg2+ concentration between dTGR and SD rats. Myocardial connective tissue growth factor (CTGF) mRNA and protein expressions were increased by 300% in dTGR (P < 0.05), especially in areas with myocardial infarctions and vascular inflammation. Magnesium supplementation prevented Ang II-induced myocardial CTGF overexpression (P < 0.05). Magnesium supplementation also improved the therapeutic effects of the calcineurin inhibitor tacrolimus, which produced marked hypomagnesemia when given as monotherapy.
Our findings suggest a salutary effect for magnesium supplementation in the treatment of Ang II-induced myocardial complications.</abstract><cop>England</cop><pmid>15662226</pmid><doi>10.1097/00004872-200502000-00020</doi><tpages>6</tpages></addata></record> |
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| subjects | Angiotensin II - pharmacology Angiotensinogen - genetics Animals Animals, Genetically Modified Blood Pressure - drug effects Cardiomegaly - therapy Connective Tissue Growth Factor Dietary Supplements Fibrosis - prevention & control Humans Immediate-Early Proteins - drug effects Immediate-Early Proteins - metabolism Immunosuppressive Agents - therapeutic use Intercellular Signaling Peptides and Proteins - metabolism Magnesium - administration & dosage Magnesium - blood Magnesium - metabolism Male Myocardium - pathology Rats Rats, Sprague-Dawley Renin - genetics RNA, Messenger - genetics RNA, Messenger - metabolism Tacrolimus - therapeutic use |
| title | Magnesium supplementation prevents angiotensin II-induced myocardial damage and CTGF overexpression |
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