Angiotensin II Stimulates Gene Expression of Cardiac Insulin-Like Growth Factor I and Its Receptor Through Effects on Blood Pressure and Food Intake
Angiotensin II (Ang II) is known to act as a growth factor and may be involved in cardiac remodeling. We have shown that insulin-like growth factor-I (IGF-I) is an autocrine mediator of growth responses to Ang II in vascular smooth muscle cells in vitro, and we hypothesized that IGF-I also serves as...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 1999-11, Vol.34 (5), p.1053-1059 |
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| creator | Brink, Marijke Chrast, Jacqueline Price, S Russ Mitch, William E Delafontaine, Patrick |
| description | Angiotensin II (Ang II) is known to act as a growth factor and may be involved in cardiac remodeling. We have shown that insulin-like growth factor-I (IGF-I) is an autocrine mediator of growth responses to Ang II in vascular smooth muscle cells in vitro, and we hypothesized that IGF-I also serves as an important modulator of cardiovascular growth in vivo. To study the effect of Ang II on cardiac IGF-I, we infused rats for 3, 7, or 14 days with Ang II through osmotic minipumps. After 7 days, left ventricular mass normalized for body weight was increased by 20% (P |
| doi_str_mv | 10.1161/01.hyp.34.5.1053 |
| format | Article |
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We have shown that insulin-like growth factor-I (IGF-I) is an autocrine mediator of growth responses to Ang II in vascular smooth muscle cells in vitro, and we hypothesized that IGF-I also serves as an important modulator of cardiovascular growth in vivo. To study the effect of Ang II on cardiac IGF-I, we infused rats for 3, 7, or 14 days with Ang II through osmotic minipumps. After 7 days, left ventricular mass normalized for body weight was increased by 20% (P<0.01) in Ang II rats compared with pair-fed control rats that were given a restricted amount of food identical to that eaten by the anorexic, Ang II-infused rats. Ang II increased left ventricular IGF-I mRNA levels by 1.5- to 1.8-fold compared with ad libitum-fed or pair-fed control rats (P<0.05). Cardiac IGF-I protein was increased correspondingly and was localized on the cardiomyocytes. Treatment with hydralazine abolished the induction of IGF-I mRNA, which indicates that Ang II induces cardiac IGF-I mRNA expression through a pressor-mediated mechanism. IGF-I receptor (IGF-IR) mRNA was induced 2.1-fold in Ang II rats compared with ad libitum-fed rats (P<0.01). However, this increase was also observed in pair-fed controls and is thus due to the anorexigenic effect of Ang II. We have recently shown that circulating IGF-I levels are reduced in response to Ang II infusion. Elevation of IGF-I levels by coinfusion of IGF-I and Ang II significantly increased left ventricular index by 16% compared with rats infused with Ang II alone (P<0.05). In conclusion, autocrine upregulation of cardiac IGF-I and IGF-IR mRNA by Ang II occurs through hemodynamic and nonhemodynamic mechanisms, respectively, and may modulate cardiac structural changes that occur in hypertension.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.34.5.1053</identifier><identifier>PMID: 10567181</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Angiotensin II - pharmacology ; Animals ; Antihypertensive Agents - pharmacology ; Biological and medical sciences ; Blood Pressure - drug effects ; Cardiology. Vascular system ; Eating - drug effects ; Heart ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hypertrophy, Left Ventricular - etiology ; Insulin-Like Growth Factor I - biosynthesis ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - pharmacology ; Male ; Medical sciences ; Myocardium - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, IGF Type 1 - genetics ; RNA, Messenger - analysis</subject><ispartof>Hypertension (Dallas, Tex. 1979), 1999-11, Vol.34 (5), p.1053-1059</ispartof><rights>1999 American Heart Association, Inc.</rights><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5466-ead450d193bb9338c8b8d105564c7f7c503eb768557a47b18fbaccded945e2c23</citedby><cites>FETCH-LOGICAL-c5466-ead450d193bb9338c8b8d105564c7f7c503eb768557a47b18fbaccded945e2c23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1187213$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10567181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brink, Marijke</creatorcontrib><creatorcontrib>Chrast, Jacqueline</creatorcontrib><creatorcontrib>Price, S Russ</creatorcontrib><creatorcontrib>Mitch, William E</creatorcontrib><creatorcontrib>Delafontaine, Patrick</creatorcontrib><title>Angiotensin II Stimulates Gene Expression of Cardiac Insulin-Like Growth Factor I and Its Receptor Through Effects on Blood Pressure and Food Intake</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Angiotensin II (Ang II) is known to act as a growth factor and may be involved in cardiac remodeling. We have shown that insulin-like growth factor-I (IGF-I) is an autocrine mediator of growth responses to Ang II in vascular smooth muscle cells in vitro, and we hypothesized that IGF-I also serves as an important modulator of cardiovascular growth in vivo. To study the effect of Ang II on cardiac IGF-I, we infused rats for 3, 7, or 14 days with Ang II through osmotic minipumps. After 7 days, left ventricular mass normalized for body weight was increased by 20% (P<0.01) in Ang II rats compared with pair-fed control rats that were given a restricted amount of food identical to that eaten by the anorexic, Ang II-infused rats. Ang II increased left ventricular IGF-I mRNA levels by 1.5- to 1.8-fold compared with ad libitum-fed or pair-fed control rats (P<0.05). Cardiac IGF-I protein was increased correspondingly and was localized on the cardiomyocytes. Treatment with hydralazine abolished the induction of IGF-I mRNA, which indicates that Ang II induces cardiac IGF-I mRNA expression through a pressor-mediated mechanism. IGF-I receptor (IGF-IR) mRNA was induced 2.1-fold in Ang II rats compared with ad libitum-fed rats (P<0.01). However, this increase was also observed in pair-fed controls and is thus due to the anorexigenic effect of Ang II. We have recently shown that circulating IGF-I levels are reduced in response to Ang II infusion. Elevation of IGF-I levels by coinfusion of IGF-I and Ang II significantly increased left ventricular index by 16% compared with rats infused with Ang II alone (P<0.05). In conclusion, autocrine upregulation of cardiac IGF-I and IGF-IR mRNA by Ang II occurs through hemodynamic and nonhemodynamic mechanisms, respectively, and may modulate cardiac structural changes that occur in hypertension.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Eating - drug effects</subject><subject>Heart</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Hypertrophy, Left Ventricular - etiology</subject><subject>Insulin-Like Growth Factor I - biosynthesis</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardium - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, IGF Type 1 - genetics</subject><subject>RNA, Messenger - analysis</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdksGL1DAYxYMo7jh69yRBxFtr0iZpe1yHmdnCgIuuoKeQpl-33ckkY9Iy7v_hH2zqDCjmEvLye48vvCD0mpKUUkE_EJr2j8c0ZylPKeH5E7SgPGMJ4yJ_ihaEViypKP12hV6E8EAIZYwVz9FVZEVBS7pAv67t_eBGsGGwuK7xl3E4TEaNEPAWLOD1z6OHEAZnsevwSvl2UBrXNkxmsMlu2APeencae7xRenQe11jZFtdjwJ9Bw3GW7nrvpvser7sOdLyIWR-Ncy2-naMnD38sm1mp7aj28BI965QJ8OqyL9HXzfpudZPsPm3r1fUu0ZwJkYBqGSctrfKmqfK81GVTtvFpXDBddIXmJIemECXnhWJFQ8uuUVq30FaMQ6azfInen3OP3v2YIIzyMAQNxigLbgpSVFklRIxZorf_gQ9u8jbOJjPCsyrjjEaInCHtXQgeOnn0w0H5R0mJnOuShMqb77cyZ5LLua5oeXPJnZoDtP8Yzv1E4N0FUEEr03ll9RD-crQsMjrnsDN2cmYEH_ZmOoGXPSgz9pLExTJRJrSq4m-Ip2SWRP4bjTitaw</recordid><startdate>199911</startdate><enddate>199911</enddate><creator>Brink, Marijke</creator><creator>Chrast, Jacqueline</creator><creator>Price, S Russ</creator><creator>Mitch, William E</creator><creator>Delafontaine, Patrick</creator><general>American Heart Association, Inc</general><general>Lippincott</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>7X8</scope></search><sort><creationdate>199911</creationdate><title>Angiotensin II Stimulates Gene Expression of Cardiac Insulin-Like Growth Factor I and Its Receptor Through Effects on Blood Pressure and Food Intake</title><author>Brink, Marijke ; Chrast, Jacqueline ; Price, S Russ ; Mitch, William E ; Delafontaine, Patrick</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5466-ead450d193bb9338c8b8d105564c7f7c503eb768557a47b18fbaccded945e2c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Eating - drug effects</topic><topic>Heart</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Hypertrophy, Left Ventricular - etiology</topic><topic>Insulin-Like Growth Factor I - biosynthesis</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Insulin-Like Growth Factor I - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardium - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, IGF Type 1 - genetics</topic><topic>RNA, Messenger - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brink, Marijke</creatorcontrib><creatorcontrib>Chrast, Jacqueline</creatorcontrib><creatorcontrib>Price, S Russ</creatorcontrib><creatorcontrib>Mitch, William E</creatorcontrib><creatorcontrib>Delafontaine, Patrick</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>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brink, Marijke</au><au>Chrast, Jacqueline</au><au>Price, S Russ</au><au>Mitch, William E</au><au>Delafontaine, Patrick</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II Stimulates Gene Expression of Cardiac Insulin-Like Growth Factor I and Its Receptor Through Effects on Blood Pressure and Food Intake</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1999-11</date><risdate>1999</risdate><volume>34</volume><issue>5</issue><spage>1053</spage><epage>1059</epage><pages>1053-1059</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Angiotensin II (Ang II) is known to act as a growth factor and may be involved in cardiac remodeling. We have shown that insulin-like growth factor-I (IGF-I) is an autocrine mediator of growth responses to Ang II in vascular smooth muscle cells in vitro, and we hypothesized that IGF-I also serves as an important modulator of cardiovascular growth in vivo. To study the effect of Ang II on cardiac IGF-I, we infused rats for 3, 7, or 14 days with Ang II through osmotic minipumps. After 7 days, left ventricular mass normalized for body weight was increased by 20% (P<0.01) in Ang II rats compared with pair-fed control rats that were given a restricted amount of food identical to that eaten by the anorexic, Ang II-infused rats. Ang II increased left ventricular IGF-I mRNA levels by 1.5- to 1.8-fold compared with ad libitum-fed or pair-fed control rats (P<0.05). Cardiac IGF-I protein was increased correspondingly and was localized on the cardiomyocytes. Treatment with hydralazine abolished the induction of IGF-I mRNA, which indicates that Ang II induces cardiac IGF-I mRNA expression through a pressor-mediated mechanism. IGF-I receptor (IGF-IR) mRNA was induced 2.1-fold in Ang II rats compared with ad libitum-fed rats (P<0.01). However, this increase was also observed in pair-fed controls and is thus due to the anorexigenic effect of Ang II. We have recently shown that circulating IGF-I levels are reduced in response to Ang II infusion. Elevation of IGF-I levels by coinfusion of IGF-I and Ang II significantly increased left ventricular index by 16% compared with rats infused with Ang II alone (P<0.05). In conclusion, autocrine upregulation of cardiac IGF-I and IGF-IR mRNA by Ang II occurs through hemodynamic and nonhemodynamic mechanisms, respectively, and may modulate cardiac structural changes that occur in hypertension.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>10567181</pmid><doi>10.1161/01.hyp.34.5.1053</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 1999-11, Vol.34 (5), p.1053-1059 |
| issn | 0194-911X 1524-4563 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Angiotensin II - pharmacology Animals Antihypertensive Agents - pharmacology Biological and medical sciences Blood Pressure - drug effects Cardiology. Vascular system Eating - drug effects Heart Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hypertrophy, Left Ventricular - etiology Insulin-Like Growth Factor I - biosynthesis Insulin-Like Growth Factor I - genetics Insulin-Like Growth Factor I - pharmacology Male Medical sciences Myocardium - metabolism Rats Rats, Sprague-Dawley Receptor, IGF Type 1 - genetics RNA, Messenger - analysis |
| title | Angiotensin II Stimulates Gene Expression of Cardiac Insulin-Like Growth Factor I and Its Receptor Through Effects on Blood Pressure and Food Intake |
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