Myocardial Stretch Stimulates Phosphatidylinositol Turnover
The mammalian myocardium responds to stretch by increasing both contractility and the release of atrial natriuretic peptide. These effects are observed in isolated perfused heart preparations as well as in vivo. That atrial natriuretic peptide release can be stimulated by activation of the phosphati...
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| Veröffentlicht in: | Circulation research 1989-08, Vol.65 (2), p.494-501 |
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| creator | von Harsdorf, Rüdiger Lang, Rudolph E Fullerton, Merryl Woodcock, Elizabeth A |
| description | The mammalian myocardium responds to stretch by increasing both contractility and the release of atrial natriuretic peptide. These effects are observed in isolated perfused heart preparations as well as in vivo. That atrial natriuretic peptide release can be stimulated by activation of the phosphatidylinositol turnover pathway suggests a possible mechanism by which stretch might activate a biological response. Accordingly, experiments were performed to examine the effect of dilatation of the right atrium on the phosphatidylinositol turnover pathway measured in isolated perfused hearts. Dilatation of the right atrium caused a stimulation of the phosphatidylinositol turnover pathway as measured by an increase in the accumulation of inositol phosphates. In right atria, increases were detected after 1 minute of dilatation, and maximal increases were observed after 10 minutes. Dilatation for 10 minutes caused an increase in inositol monophosphate, inositol bisphosphate, and inositol trisphosphate from 23.3±0.9, 15.4±0.4, and 9.5±0.3 cpm/mg tissue (mean±SEM, n=7) to 74.6±2.3, 20.2±1.3, and 13.6±1.5 cpm/mg tissue (n=8), respectively (p |
| doi_str_mv | 10.1161/01.RES.65.2.494 |
| format | Article |
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These effects are observed in isolated perfused heart preparations as well as in vivo. That atrial natriuretic peptide release can be stimulated by activation of the phosphatidylinositol turnover pathway suggests a possible mechanism by which stretch might activate a biological response. Accordingly, experiments were performed to examine the effect of dilatation of the right atrium on the phosphatidylinositol turnover pathway measured in isolated perfused hearts. Dilatation of the right atrium caused a stimulation of the phosphatidylinositol turnover pathway as measured by an increase in the accumulation of inositol phosphates. In right atria, increases were detected after 1 minute of dilatation, and maximal increases were observed after 10 minutes. Dilatation for 10 minutes caused an increase in inositol monophosphate, inositol bisphosphate, and inositol trisphosphate from 23.3±0.9, 15.4±0.4, and 9.5±0.3 cpm/mg tissue (mean±SEM, n=7) to 74.6±2.3, 20.2±1.3, and 13.6±1.5 cpm/mg tissue (n=8), respectively (p<0.01 for all inositol phosphates). Smaller increases were observed in the other chambers of the hearts. Perfusion with propranolol, prazosin, and atropine (all 1 μM) did not alter the inositol phosphate response to dilatation, indicating that it was not secondary to release of norepinephrine or acetylcholine. Dilatation of the right ventricle also caused a stimulation of inositol phosphate accumulation, but this was lower than after dilatation of the right atrium. These results show that the myocardium can respond to dilatation by an activation of the phosphatidylinositol turnover pathway. Such a mechanism has implications for the release of atrial natriuretic peptide and also provides a potential mechanism for the enhanced contractility after increased venous return. (Circulation Research 1989;65:494-501)</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.65.2.494</identifier><identifier>PMID: 2752554</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Biological and medical sciences ; Dilatation ; Fundamental and applied biological sciences. Psychology ; Heart ; Heart Atria ; Heart Ventricles ; Male ; Myocardial Contraction ; Myocardium - metabolism ; Norepinephrine - pharmacology ; Parasympatholytics - pharmacology ; Perfusion ; Phosphatidylinositols - metabolism ; Physical Stimulation ; Rats ; Rats, Inbred Strains ; Sympatholytics - pharmacology ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 1989-08, Vol.65 (2), p.494-501</ispartof><rights>1989 American Heart Association, Inc.</rights><rights>1990 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4437-981abdfb5a613af91a62528eaabba4711e48dfb2f7440d1a73bd8bdccdaa87dc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=6963389$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2752554$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>von Harsdorf, Rüdiger</creatorcontrib><creatorcontrib>Lang, Rudolph E</creatorcontrib><creatorcontrib>Fullerton, Merryl</creatorcontrib><creatorcontrib>Woodcock, Elizabeth A</creatorcontrib><title>Myocardial Stretch Stimulates Phosphatidylinositol Turnover</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>The mammalian myocardium responds to stretch by increasing both contractility and the release of atrial natriuretic peptide. These effects are observed in isolated perfused heart preparations as well as in vivo. That atrial natriuretic peptide release can be stimulated by activation of the phosphatidylinositol turnover pathway suggests a possible mechanism by which stretch might activate a biological response. Accordingly, experiments were performed to examine the effect of dilatation of the right atrium on the phosphatidylinositol turnover pathway measured in isolated perfused hearts. Dilatation of the right atrium caused a stimulation of the phosphatidylinositol turnover pathway as measured by an increase in the accumulation of inositol phosphates. In right atria, increases were detected after 1 minute of dilatation, and maximal increases were observed after 10 minutes. Dilatation for 10 minutes caused an increase in inositol monophosphate, inositol bisphosphate, and inositol trisphosphate from 23.3±0.9, 15.4±0.4, and 9.5±0.3 cpm/mg tissue (mean±SEM, n=7) to 74.6±2.3, 20.2±1.3, and 13.6±1.5 cpm/mg tissue (n=8), respectively (p<0.01 for all inositol phosphates). Smaller increases were observed in the other chambers of the hearts. Perfusion with propranolol, prazosin, and atropine (all 1 μM) did not alter the inositol phosphate response to dilatation, indicating that it was not secondary to release of norepinephrine or acetylcholine. Dilatation of the right ventricle also caused a stimulation of inositol phosphate accumulation, but this was lower than after dilatation of the right atrium. These results show that the myocardium can respond to dilatation by an activation of the phosphatidylinositol turnover pathway. Such a mechanism has implications for the release of atrial natriuretic peptide and also provides a potential mechanism for the enhanced contractility after increased venous return. (Circulation Research 1989;65:494-501)</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Dilatation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Heart Atria</subject><subject>Heart Ventricles</subject><subject>Male</subject><subject>Myocardial Contraction</subject><subject>Myocardium - metabolism</subject><subject>Norepinephrine - pharmacology</subject><subject>Parasympatholytics - pharmacology</subject><subject>Perfusion</subject><subject>Phosphatidylinositols - metabolism</subject><subject>Physical Stimulation</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Sympatholytics - pharmacology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kc1r3DAQxUVJSbdpzj0V9hB6s6PRh2WRUwlJE0hJ6CZnMZZk7Ea72kp2l_3vo7JLDsNjeL95hzeEfAVaAzRwSaH-fbOqG1mzWmjxgSxAMlEJqeCELCilulKc00_kc85_KAXBmT4lp0xJJqVYkKtf-2gxuRHDcjUlP9mh6LieA04-L5-GmLcDTqPbh3ET8zjFsHye0yb-8-kL-dhjyP78qGfk5fbm-fquenj8eX_946GyQnBV6Rawc30nsQGOvQZsmGStR-w6FArAi7bYrFdCUAeoeOfazlnrEFvlLD8j3w-52xT_zj5PZj1m60PAjY9zNkoDE0yJAl4eQJtizsn3ZpvGNaa9AWr-12UomFKXaaRhptRVLr4do-du7d07f-yn-BdHH7PF0Cfc2DG_Y41uOG91wcQB28Uw-ZRfw7zzyQwewzSY8gXKKbAKdKtpW7aqDFP8DXoOg6E</recordid><startdate>198908</startdate><enddate>198908</enddate><creator>von Harsdorf, Rüdiger</creator><creator>Lang, Rudolph E</creator><creator>Fullerton, Merryl</creator><creator>Woodcock, Elizabeth A</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>7X8</scope></search><sort><creationdate>198908</creationdate><title>Myocardial Stretch Stimulates Phosphatidylinositol Turnover</title><author>von Harsdorf, Rüdiger ; Lang, Rudolph E ; Fullerton, Merryl ; Woodcock, Elizabeth A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4437-981abdfb5a613af91a62528eaabba4711e48dfb2f7440d1a73bd8bdccdaa87dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Dilatation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart</topic><topic>Heart Atria</topic><topic>Heart Ventricles</topic><topic>Male</topic><topic>Myocardial Contraction</topic><topic>Myocardium - metabolism</topic><topic>Norepinephrine - pharmacology</topic><topic>Parasympatholytics - pharmacology</topic><topic>Perfusion</topic><topic>Phosphatidylinositols - metabolism</topic><topic>Physical Stimulation</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Sympatholytics - pharmacology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>von Harsdorf, Rüdiger</creatorcontrib><creatorcontrib>Lang, Rudolph E</creatorcontrib><creatorcontrib>Fullerton, Merryl</creatorcontrib><creatorcontrib>Woodcock, Elizabeth A</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>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>von Harsdorf, Rüdiger</au><au>Lang, Rudolph E</au><au>Fullerton, Merryl</au><au>Woodcock, Elizabeth A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial Stretch Stimulates Phosphatidylinositol Turnover</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1989-08</date><risdate>1989</risdate><volume>65</volume><issue>2</issue><spage>494</spage><epage>501</epage><pages>494-501</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>The mammalian myocardium responds to stretch by increasing both contractility and the release of atrial natriuretic peptide. These effects are observed in isolated perfused heart preparations as well as in vivo. That atrial natriuretic peptide release can be stimulated by activation of the phosphatidylinositol turnover pathway suggests a possible mechanism by which stretch might activate a biological response. Accordingly, experiments were performed to examine the effect of dilatation of the right atrium on the phosphatidylinositol turnover pathway measured in isolated perfused hearts. Dilatation of the right atrium caused a stimulation of the phosphatidylinositol turnover pathway as measured by an increase in the accumulation of inositol phosphates. In right atria, increases were detected after 1 minute of dilatation, and maximal increases were observed after 10 minutes. Dilatation for 10 minutes caused an increase in inositol monophosphate, inositol bisphosphate, and inositol trisphosphate from 23.3±0.9, 15.4±0.4, and 9.5±0.3 cpm/mg tissue (mean±SEM, n=7) to 74.6±2.3, 20.2±1.3, and 13.6±1.5 cpm/mg tissue (n=8), respectively (p<0.01 for all inositol phosphates). Smaller increases were observed in the other chambers of the hearts. Perfusion with propranolol, prazosin, and atropine (all 1 μM) did not alter the inositol phosphate response to dilatation, indicating that it was not secondary to release of norepinephrine or acetylcholine. Dilatation of the right ventricle also caused a stimulation of inositol phosphate accumulation, but this was lower than after dilatation of the right atrium. These results show that the myocardium can respond to dilatation by an activation of the phosphatidylinositol turnover pathway. Such a mechanism has implications for the release of atrial natriuretic peptide and also provides a potential mechanism for the enhanced contractility after increased venous return. (Circulation Research 1989;65:494-501)</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>2752554</pmid><doi>10.1161/01.RES.65.2.494</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation research, 1989-08, Vol.65 (2), p.494-501 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Ovid Autoload |
| subjects | Animals Biological and medical sciences Dilatation Fundamental and applied biological sciences. Psychology Heart Heart Atria Heart Ventricles Male Myocardial Contraction Myocardium - metabolism Norepinephrine - pharmacology Parasympatholytics - pharmacology Perfusion Phosphatidylinositols - metabolism Physical Stimulation Rats Rats, Inbred Strains Sympatholytics - pharmacology Vertebrates: cardiovascular system |
| title | Myocardial Stretch Stimulates Phosphatidylinositol Turnover |
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