Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure
Adrenomedullin (AM) is a potent vasorelaxing peptide with natriuretic, diuretic, and growth inhibitory properties. Plasma concentrations and myocardial AM expression are increased in heart failure (HF). Since AM and AM binding sites are abundantly expressed in the lungs, we investigated to what exte...
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| Veröffentlicht in: | Basic research in cardiology 2010, Vol.105 (1), p.89-98 |
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| creator | Øie, Erik Ahmed, Mohammed Shakil Ueland, Thor Sikkeland, Liv Ingunn Bjoner Dahl, Christen P. Hagelin, Else Marie Valbjørn von Lueder, Thomas Edvardsen, Thor Andreassen, Arne K. Gullestad, Lars Aukrust, Pål Yndestad, Arne Vinge, Leif Erik Attramadal, Håvard |
| description | Adrenomedullin (AM) is a potent vasorelaxing peptide with natriuretic, diuretic, and growth inhibitory properties. Plasma concentrations and myocardial AM expression are increased in heart failure (HF). Since AM and AM binding sites are abundantly expressed in the lungs, we investigated to what extent pulmonary AM and AM receptor subtypes [CRLR/RAMP2 (AM
1
) and CRLR/RAMP3 (AM
2
)] are changed in HF and whether the lungs contribute to the increased plasma concentrations of AM reported in HF. Pulmonary AM mRNA and protein expression were increased by 2.8- and 2.6-fold, respectively, whereas mRNA expression of RAMP2 and CRLR was decreased in rats with HF 7 days after induction of MI compared to sham-operated rats (
P
|
| doi_str_mv | 10.1007/s00395-009-0070-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_734220177</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1917785781</sourcerecordid><originalsourceid>FETCH-LOGICAL-c401t-ade467eecc3c38408525d9dce66b6c1a128bd9b37900070d1a93ce41a85d0b9a3</originalsourceid><addsrcrecordid>eNp9kU9r3DAQxUVpaDZpP0AvRfTQnNzOSP4jH0No0kKgl_QsZGl210GWt5IdWMiHr1wvBArtQUiDfvNGeo-x9wifEaD5kgBkWxUAbV4NFMdXbIOlrApUIF-zDUiAQpVCnbOLlB4BsKxrfMPOsVVCqhY37PnaRQrjQG72vg-8T7wPNpJJ5PKJG_9EozeRD8bG8bA3O0rcBMcj-RXaxnHg0564n8Nu6Z7GP6Xto529mfoxLEKJnigS35OJE9-a3s-R3rKzrfGJ3p32S_bz9uvDzbfi_sfd95vr-8KWgFNhHJV1Q2SttFKVoCpRudZZquuutmhQqM61nWxaWGxwaFppqUSjKgdda-Qlu1p1D3H8NVOa9NAnS96bQOOcdCNLIQCbJpOf_kuKPEtViBn8-Bf4OM4x5F9kRiJkg0WGcIWydSlF2upD7AcTjxpBLwnqNUGdE9TL0_Ux93w4Cc9dTuWl4xRZBsQKpHwVdhRfJv9b9TctPKg-</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>213109822</pqid></control><display><type>article</type><title>Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Øie, Erik ; Ahmed, Mohammed Shakil ; Ueland, Thor ; Sikkeland, Liv Ingunn Bjoner ; Dahl, Christen P. ; Hagelin, Else Marie Valbjørn ; von Lueder, Thomas ; Edvardsen, Thor ; Andreassen, Arne K. ; Gullestad, Lars ; Aukrust, Pål ; Yndestad, Arne ; Vinge, Leif Erik ; Attramadal, Håvard</creator><creatorcontrib>Øie, Erik ; Ahmed, Mohammed Shakil ; Ueland, Thor ; Sikkeland, Liv Ingunn Bjoner ; Dahl, Christen P. ; Hagelin, Else Marie Valbjørn ; von Lueder, Thomas ; Edvardsen, Thor ; Andreassen, Arne K. ; Gullestad, Lars ; Aukrust, Pål ; Yndestad, Arne ; Vinge, Leif Erik ; Attramadal, Håvard</creatorcontrib><description>Adrenomedullin (AM) is a potent vasorelaxing peptide with natriuretic, diuretic, and growth inhibitory properties. Plasma concentrations and myocardial AM expression are increased in heart failure (HF). Since AM and AM binding sites are abundantly expressed in the lungs, we investigated to what extent pulmonary AM and AM receptor subtypes [CRLR/RAMP2 (AM
1
) and CRLR/RAMP3 (AM
2
)] are changed in HF and whether the lungs contribute to the increased plasma concentrations of AM reported in HF. Pulmonary AM mRNA and protein expression were increased by 2.8- and 2.6-fold, respectively, whereas mRNA expression of RAMP2 and CRLR was decreased in rats with HF 7 days after induction of MI compared to sham-operated rats (
P
< 0.05). Pulmonary AM receptor density was substantially decreased in HF rats compared to sham (3.7 ± 0.6 vs. 29.9 ± 1.1 fmol/mg membrane protein;
P
< 0.05). Immunoreactivities against AM and the AM receptor components CRLR, RAMP2, and RAMP3 in the pulmonary tissue were seen in vascular smooth muscle cells, vascular endothelial cells, and in alveolar macrophages. AM mRNA expression in alveolar macrophages obtained from HF rats by bronchoalveolar lavage was 2.9-fold higher than in sham-operated rats (
P
< 0.05). An even more substantial increase of AM mRNA expression was found in alveolar macrophages from patients with HF (10-fold,
P
< 0.05), and this increase displayed a negative correlation to left ventricular systolic function (
P
< 0.05). Furthermore, a net release of AM from the lungs into the circulation was only found in HF patients with the most severe left ventricular systolic dysfunction. Thus, our data demonstrate increased expression and decreased receptor binding of AM in the lungs in severe HF. Furthermore, our data indicate that alveolar macrophages are an important source of pulmonary AM in both experimental and clinical HF. Finally, a net release of AM from the lungs into the circulation was only found in patients with severe systolic dysfunction.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/s00395-009-0070-y</identifier><identifier>PMID: 19823891</identifier><language>eng</language><publisher>Heidelberg: D. Steinkopff-Verlag</publisher><subject>Adrenomedullin - metabolism ; Animals ; Binding Sites ; Blood Pressure ; Calcitonin Receptor-Like Protein ; Cardiology ; Gene Expression ; Heart Failure - immunology ; Heart Failure - metabolism ; Heart Failure - physiopathology ; Humans ; Immunohistochemistry ; Intracellular Signaling Peptides and Proteins - metabolism ; Lung - metabolism ; Lung - pathology ; Macrophages, Alveolar - metabolism ; Male ; Medicine ; Medicine & Public Health ; Membrane Proteins - metabolism ; Myocardial Infarction - metabolism ; Myocardial Infarction - physiopathology ; Myocardium - pathology ; Organ Size ; Original Contribution ; Rats ; Rats, Wistar ; Receptor Activity-Modifying Protein 2 ; Receptor Activity-Modifying Protein 3 ; Receptor Activity-Modifying Proteins ; Receptors, Adrenomedullin ; Receptors, Calcitonin - metabolism ; Receptors, Peptide - metabolism ; RNA, Messenger - metabolism ; Systole ; Ventricular Function, Left</subject><ispartof>Basic research in cardiology, 2010, Vol.105 (1), p.89-98</ispartof><rights>Springer-Verlag 2009</rights><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-ade467eecc3c38408525d9dce66b6c1a128bd9b37900070d1a93ce41a85d0b9a3</citedby><cites>FETCH-LOGICAL-c401t-ade467eecc3c38408525d9dce66b6c1a128bd9b37900070d1a93ce41a85d0b9a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00395-009-0070-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00395-009-0070-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19823891$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Øie, Erik</creatorcontrib><creatorcontrib>Ahmed, Mohammed Shakil</creatorcontrib><creatorcontrib>Ueland, Thor</creatorcontrib><creatorcontrib>Sikkeland, Liv Ingunn Bjoner</creatorcontrib><creatorcontrib>Dahl, Christen P.</creatorcontrib><creatorcontrib>Hagelin, Else Marie Valbjørn</creatorcontrib><creatorcontrib>von Lueder, Thomas</creatorcontrib><creatorcontrib>Edvardsen, Thor</creatorcontrib><creatorcontrib>Andreassen, Arne K.</creatorcontrib><creatorcontrib>Gullestad, Lars</creatorcontrib><creatorcontrib>Aukrust, Pål</creatorcontrib><creatorcontrib>Yndestad, Arne</creatorcontrib><creatorcontrib>Vinge, Leif Erik</creatorcontrib><creatorcontrib>Attramadal, Håvard</creatorcontrib><title>Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><addtitle>Basic Res Cardiol</addtitle><description>Adrenomedullin (AM) is a potent vasorelaxing peptide with natriuretic, diuretic, and growth inhibitory properties. Plasma concentrations and myocardial AM expression are increased in heart failure (HF). Since AM and AM binding sites are abundantly expressed in the lungs, we investigated to what extent pulmonary AM and AM receptor subtypes [CRLR/RAMP2 (AM
1
) and CRLR/RAMP3 (AM
2
)] are changed in HF and whether the lungs contribute to the increased plasma concentrations of AM reported in HF. Pulmonary AM mRNA and protein expression were increased by 2.8- and 2.6-fold, respectively, whereas mRNA expression of RAMP2 and CRLR was decreased in rats with HF 7 days after induction of MI compared to sham-operated rats (
P
< 0.05). Pulmonary AM receptor density was substantially decreased in HF rats compared to sham (3.7 ± 0.6 vs. 29.9 ± 1.1 fmol/mg membrane protein;
P
< 0.05). Immunoreactivities against AM and the AM receptor components CRLR, RAMP2, and RAMP3 in the pulmonary tissue were seen in vascular smooth muscle cells, vascular endothelial cells, and in alveolar macrophages. AM mRNA expression in alveolar macrophages obtained from HF rats by bronchoalveolar lavage was 2.9-fold higher than in sham-operated rats (
P
< 0.05). An even more substantial increase of AM mRNA expression was found in alveolar macrophages from patients with HF (10-fold,
P
< 0.05), and this increase displayed a negative correlation to left ventricular systolic function (
P
< 0.05). Furthermore, a net release of AM from the lungs into the circulation was only found in HF patients with the most severe left ventricular systolic dysfunction. Thus, our data demonstrate increased expression and decreased receptor binding of AM in the lungs in severe HF. Furthermore, our data indicate that alveolar macrophages are an important source of pulmonary AM in both experimental and clinical HF. Finally, a net release of AM from the lungs into the circulation was only found in patients with severe systolic dysfunction.</description><subject>Adrenomedullin - metabolism</subject><subject>Animals</subject><subject>Binding Sites</subject><subject>Blood Pressure</subject><subject>Calcitonin Receptor-Like Protein</subject><subject>Cardiology</subject><subject>Gene Expression</subject><subject>Heart Failure - immunology</subject><subject>Heart Failure - metabolism</subject><subject>Heart Failure - physiopathology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane Proteins - metabolism</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardium - pathology</subject><subject>Organ Size</subject><subject>Original Contribution</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor Activity-Modifying Protein 2</subject><subject>Receptor Activity-Modifying Protein 3</subject><subject>Receptor Activity-Modifying Proteins</subject><subject>Receptors, Adrenomedullin</subject><subject>Receptors, Calcitonin - metabolism</subject><subject>Receptors, Peptide - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Systole</subject><subject>Ventricular Function, Left</subject><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kU9r3DAQxUVpaDZpP0AvRfTQnNzOSP4jH0No0kKgl_QsZGl210GWt5IdWMiHr1wvBArtQUiDfvNGeo-x9wifEaD5kgBkWxUAbV4NFMdXbIOlrApUIF-zDUiAQpVCnbOLlB4BsKxrfMPOsVVCqhY37PnaRQrjQG72vg-8T7wPNpJJ5PKJG_9EozeRD8bG8bA3O0rcBMcj-RXaxnHg0564n8Nu6Z7GP6Xto529mfoxLEKJnigS35OJE9-a3s-R3rKzrfGJ3p32S_bz9uvDzbfi_sfd95vr-8KWgFNhHJV1Q2SttFKVoCpRudZZquuutmhQqM61nWxaWGxwaFppqUSjKgdda-Qlu1p1D3H8NVOa9NAnS96bQOOcdCNLIQCbJpOf_kuKPEtViBn8-Bf4OM4x5F9kRiJkg0WGcIWydSlF2upD7AcTjxpBLwnqNUGdE9TL0_Ux93w4Cc9dTuWl4xRZBsQKpHwVdhRfJv9b9TctPKg-</recordid><startdate>2010</startdate><enddate>2010</enddate><creator>Øie, Erik</creator><creator>Ahmed, Mohammed Shakil</creator><creator>Ueland, Thor</creator><creator>Sikkeland, Liv Ingunn Bjoner</creator><creator>Dahl, Christen P.</creator><creator>Hagelin, Else Marie Valbjørn</creator><creator>von Lueder, Thomas</creator><creator>Edvardsen, Thor</creator><creator>Andreassen, Arne K.</creator><creator>Gullestad, Lars</creator><creator>Aukrust, Pål</creator><creator>Yndestad, Arne</creator><creator>Vinge, Leif Erik</creator><creator>Attramadal, Håvard</creator><general>D. Steinkopff-Verlag</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>2010</creationdate><title>Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure</title><author>Øie, Erik ; Ahmed, Mohammed Shakil ; Ueland, Thor ; Sikkeland, Liv Ingunn Bjoner ; Dahl, Christen P. ; Hagelin, Else Marie Valbjørn ; von Lueder, Thomas ; Edvardsen, Thor ; Andreassen, Arne K. ; Gullestad, Lars ; Aukrust, Pål ; Yndestad, Arne ; Vinge, Leif Erik ; Attramadal, Håvard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-ade467eecc3c38408525d9dce66b6c1a128bd9b37900070d1a93ce41a85d0b9a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adrenomedullin - metabolism</topic><topic>Animals</topic><topic>Binding Sites</topic><topic>Blood Pressure</topic><topic>Calcitonin Receptor-Like Protein</topic><topic>Cardiology</topic><topic>Gene Expression</topic><topic>Heart Failure - immunology</topic><topic>Heart Failure - metabolism</topic><topic>Heart Failure - physiopathology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Membrane Proteins - metabolism</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardium - pathology</topic><topic>Organ Size</topic><topic>Original Contribution</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor Activity-Modifying Protein 2</topic><topic>Receptor Activity-Modifying Protein 3</topic><topic>Receptor Activity-Modifying Proteins</topic><topic>Receptors, Adrenomedullin</topic><topic>Receptors, Calcitonin - metabolism</topic><topic>Receptors, Peptide - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Systole</topic><topic>Ventricular Function, Left</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Øie, Erik</creatorcontrib><creatorcontrib>Ahmed, Mohammed Shakil</creatorcontrib><creatorcontrib>Ueland, Thor</creatorcontrib><creatorcontrib>Sikkeland, Liv Ingunn Bjoner</creatorcontrib><creatorcontrib>Dahl, Christen P.</creatorcontrib><creatorcontrib>Hagelin, Else Marie Valbjørn</creatorcontrib><creatorcontrib>von Lueder, Thomas</creatorcontrib><creatorcontrib>Edvardsen, Thor</creatorcontrib><creatorcontrib>Andreassen, Arne K.</creatorcontrib><creatorcontrib>Gullestad, Lars</creatorcontrib><creatorcontrib>Aukrust, Pål</creatorcontrib><creatorcontrib>Yndestad, Arne</creatorcontrib><creatorcontrib>Vinge, Leif Erik</creatorcontrib><creatorcontrib>Attramadal, Håvard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Basic research in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Øie, Erik</au><au>Ahmed, Mohammed Shakil</au><au>Ueland, Thor</au><au>Sikkeland, Liv Ingunn Bjoner</au><au>Dahl, Christen P.</au><au>Hagelin, Else Marie Valbjørn</au><au>von Lueder, Thomas</au><au>Edvardsen, Thor</au><au>Andreassen, Arne K.</au><au>Gullestad, Lars</au><au>Aukrust, Pål</au><au>Yndestad, Arne</au><au>Vinge, Leif Erik</au><au>Attramadal, Håvard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure</atitle><jtitle>Basic research in cardiology</jtitle><stitle>Basic Res Cardiol</stitle><addtitle>Basic Res Cardiol</addtitle><date>2010</date><risdate>2010</risdate><volume>105</volume><issue>1</issue><spage>89</spage><epage>98</epage><pages>89-98</pages><issn>0300-8428</issn><eissn>1435-1803</eissn><abstract>Adrenomedullin (AM) is a potent vasorelaxing peptide with natriuretic, diuretic, and growth inhibitory properties. Plasma concentrations and myocardial AM expression are increased in heart failure (HF). Since AM and AM binding sites are abundantly expressed in the lungs, we investigated to what extent pulmonary AM and AM receptor subtypes [CRLR/RAMP2 (AM
1
) and CRLR/RAMP3 (AM
2
)] are changed in HF and whether the lungs contribute to the increased plasma concentrations of AM reported in HF. Pulmonary AM mRNA and protein expression were increased by 2.8- and 2.6-fold, respectively, whereas mRNA expression of RAMP2 and CRLR was decreased in rats with HF 7 days after induction of MI compared to sham-operated rats (
P
< 0.05). Pulmonary AM receptor density was substantially decreased in HF rats compared to sham (3.7 ± 0.6 vs. 29.9 ± 1.1 fmol/mg membrane protein;
P
< 0.05). Immunoreactivities against AM and the AM receptor components CRLR, RAMP2, and RAMP3 in the pulmonary tissue were seen in vascular smooth muscle cells, vascular endothelial cells, and in alveolar macrophages. AM mRNA expression in alveolar macrophages obtained from HF rats by bronchoalveolar lavage was 2.9-fold higher than in sham-operated rats (
P
< 0.05). An even more substantial increase of AM mRNA expression was found in alveolar macrophages from patients with HF (10-fold,
P
< 0.05), and this increase displayed a negative correlation to left ventricular systolic function (
P
< 0.05). Furthermore, a net release of AM from the lungs into the circulation was only found in HF patients with the most severe left ventricular systolic dysfunction. Thus, our data demonstrate increased expression and decreased receptor binding of AM in the lungs in severe HF. Furthermore, our data indicate that alveolar macrophages are an important source of pulmonary AM in both experimental and clinical HF. Finally, a net release of AM from the lungs into the circulation was only found in patients with severe systolic dysfunction.</abstract><cop>Heidelberg</cop><pub>D. Steinkopff-Verlag</pub><pmid>19823891</pmid><doi>10.1007/s00395-009-0070-y</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-8428 |
| ispartof | Basic research in cardiology, 2010, Vol.105 (1), p.89-98 |
| issn | 0300-8428 1435-1803 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Adrenomedullin - metabolism Animals Binding Sites Blood Pressure Calcitonin Receptor-Like Protein Cardiology Gene Expression Heart Failure - immunology Heart Failure - metabolism Heart Failure - physiopathology Humans Immunohistochemistry Intracellular Signaling Peptides and Proteins - metabolism Lung - metabolism Lung - pathology Macrophages, Alveolar - metabolism Male Medicine Medicine & Public Health Membrane Proteins - metabolism Myocardial Infarction - metabolism Myocardial Infarction - physiopathology Myocardium - pathology Organ Size Original Contribution Rats Rats, Wistar Receptor Activity-Modifying Protein 2 Receptor Activity-Modifying Protein 3 Receptor Activity-Modifying Proteins Receptors, Adrenomedullin Receptors, Calcitonin - metabolism Receptors, Peptide - metabolism RNA, Messenger - metabolism Systole Ventricular Function, Left |
| title | Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure |
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