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Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway
Myocardial sympathetic activity is increased in heart failure. We tested the hypothesis that norepinephrine (NE) stimulates apoptosis in adult rat ventricular myocytes in vitro. Myocytes were exposed to NE alone (10 micromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoprot...
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| Published in: | Circulation (New York, N.Y.) N.Y.), 1998-09, Vol.98 (13), p.1329-1334 |
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| Main Authors: | , , , |
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| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c368t-a725125b6c6cea840061a0fb827d669b7eccaf7751059b5e63c9a1f0a05bd1c53 |
| container_end_page | 1334 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | COMMUNAL, C SINGH, K PIMENTEL, D. R COLUCCI, W. S |
| description | Myocardial sympathetic activity is increased in heart failure. We tested the hypothesis that norepinephrine (NE) stimulates apoptosis in adult rat ventricular myocytes in vitro.
Myocytes were exposed to NE alone (10 micromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoproterenol (ISO, 10 micromol/L) for 24 hours. NE and ISO decreased the number of viable myocytes by approximately 35%. This effect was completely blocked by the beta-adrenergic antagonist propranolol but was not affected by the alpha1-adrenergic antagonist prazosin. NE increased DNA laddering on agarose gel electrophoresis and increased the percentage of cells that were stained by terminal deoxynucleotidyl transferase-mediated nick end-labeling from 5.8+/-1. 0% to 21.0+/-2.3% (P |
| doi_str_mv | 10.1161/01.CIR.98.13.1329 |
| format | article |
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Myocytes were exposed to NE alone (10 micromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoproterenol (ISO, 10 micromol/L) for 24 hours. NE and ISO decreased the number of viable myocytes by approximately 35%. This effect was completely blocked by the beta-adrenergic antagonist propranolol but was not affected by the alpha1-adrenergic antagonist prazosin. NE increased DNA laddering on agarose gel electrophoresis and increased the percentage of cells that were stained by terminal deoxynucleotidyl transferase-mediated nick end-labeling from 5.8+/-1. 0% to 21.0+/-2.3% (P<0.01; n=4). NE likewise increased the percentage of apoptotic cells with hypodiploid DNA content as assessed by flow cytometry from 7.8+/-0.7% to 16.7+/-2.2% (P<0.01; n=6), and this effect was abolished by propranolol but not prazosin. ISO and forskolin (10 micromol/L) mimicked the effect of NE, increasing the percentage of apoptotic cells to 14.7+/-1.9% and 14. 4+/-2.2%, respectively. NE-stimulated apoptosis was abolished by the protein kinase A inhibitor H-89 (20 micromol/L) or the voltage-dependent calcium channel blockers diltiazem and nifedipine.
NE, acting via the ss-adrenergic pathway, stimulates apoptosis in adult rat cardiac myocytes in vitro. This effect is mediated by protein kinase A and requires calcium entry via voltage-dependent calcium channels. NE-stimulated apoptosis of cardiac myocytes may contribute to the progression of myocardial failure.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.98.13.1329</identifier><identifier>PMID: 9751683</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adenylyl Cyclases - physiology ; Animals ; Apoptosis - drug effects ; Biological and medical sciences ; Calcium Channels - physiology ; Cardiology. Vascular system ; Cells, Cultured ; Cyclic AMP-Dependent Protein Kinases - physiology ; Flow Cytometry ; Heart ; Heart - drug effects ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Isoproterenol - pharmacology ; Male ; Medical sciences ; Myocardium - cytology ; Norepinephrine - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta - drug effects</subject><ispartof>Circulation (New York, N.Y.), 1998-09, Vol.98 (13), p.1329-1334</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-a725125b6c6cea840061a0fb827d669b7eccaf7751059b5e63c9a1f0a05bd1c53</citedby><cites>FETCH-LOGICAL-c368t-a725125b6c6cea840061a0fb827d669b7eccaf7751059b5e63c9a1f0a05bd1c53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2400234$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9751683$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>COMMUNAL, C</creatorcontrib><creatorcontrib>SINGH, K</creatorcontrib><creatorcontrib>PIMENTEL, D. R</creatorcontrib><creatorcontrib>COLUCCI, W. S</creatorcontrib><title>Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Myocardial sympathetic activity is increased in heart failure. We tested the hypothesis that norepinephrine (NE) stimulates apoptosis in adult rat ventricular myocytes in vitro.
Myocytes were exposed to NE alone (10 micromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoproterenol (ISO, 10 micromol/L) for 24 hours. NE and ISO decreased the number of viable myocytes by approximately 35%. This effect was completely blocked by the beta-adrenergic antagonist propranolol but was not affected by the alpha1-adrenergic antagonist prazosin. NE increased DNA laddering on agarose gel electrophoresis and increased the percentage of cells that were stained by terminal deoxynucleotidyl transferase-mediated nick end-labeling from 5.8+/-1. 0% to 21.0+/-2.3% (P<0.01; n=4). NE likewise increased the percentage of apoptotic cells with hypodiploid DNA content as assessed by flow cytometry from 7.8+/-0.7% to 16.7+/-2.2% (P<0.01; n=6), and this effect was abolished by propranolol but not prazosin. ISO and forskolin (10 micromol/L) mimicked the effect of NE, increasing the percentage of apoptotic cells to 14.7+/-1.9% and 14. 4+/-2.2%, respectively. NE-stimulated apoptosis was abolished by the protein kinase A inhibitor H-89 (20 micromol/L) or the voltage-dependent calcium channel blockers diltiazem and nifedipine.
NE, acting via the ss-adrenergic pathway, stimulates apoptosis in adult rat cardiac myocytes in vitro. This effect is mediated by protein kinase A and requires calcium entry via voltage-dependent calcium channels. NE-stimulated apoptosis of cardiac myocytes may contribute to the progression of myocardial failure.</description><subject>Adenylyl Cyclases - physiology</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Calcium Channels - physiology</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Cyclic AMP-Dependent Protein Kinases - physiology</subject><subject>Flow Cytometry</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Isoproterenol - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardium - cytology</subject><subject>Norepinephrine - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Adrenergic, beta - drug effects</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNo9kM1qGzEQx0VJcR23D5BDQYeQ2zr6sLSrYzFJazAJlOYsZrXaWmF3tZW0LvtaeZA-U2ViDMMMw_zm64_QDSVrSiW9J3S93f1cq2pNeTamPqAlFWxTbARXV2hJCFFFyRn7hK5jfM2p5KVYoIUqBZUVX6LxyQc7usGOh5A9jsn1UwfJRgyjH5OPLmI3YGimLuEACR_tkIIzGQq4n72ZT2w9YzDJHSE5P2Df4nSw-N9bAU2wgw2_ncEjpMNfmD-jjy100X45xxV6eXz4tf1R7J-_77bf9oXhskoFlExQJmpppLFQbfLlFEhbV6xspFR1aY2BtsxvEKFqYSU3CmhLgIi6oUbwFbp7nzsG_2eyMeneRWO7Dgbrp6hLrliVN2SQvoMm-BiDbfUYXA9h1pTok8qaUJ1V1qrSlOuTyrnn63n4VPe2uXScZc3123MdooGuDTAYFy8Yy-8wvuH_AdUZiD0</recordid><startdate>19980929</startdate><enddate>19980929</enddate><creator>COMMUNAL, C</creator><creator>SINGH, K</creator><creator>PIMENTEL, D. R</creator><creator>COLUCCI, W. S</creator><general>Lippincott Williams & Wilkins</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>19980929</creationdate><title>Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway</title><author>COMMUNAL, C ; SINGH, K ; PIMENTEL, D. R ; COLUCCI, W. S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c368t-a725125b6c6cea840061a0fb827d669b7eccaf7751059b5e63c9a1f0a05bd1c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adenylyl Cyclases - physiology</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Calcium Channels - physiology</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Cyclic AMP-Dependent Protein Kinases - physiology</topic><topic>Flow Cytometry</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Isoproterenol - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardium - cytology</topic><topic>Norepinephrine - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Adrenergic, beta - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>COMMUNAL, C</creatorcontrib><creatorcontrib>SINGH, K</creatorcontrib><creatorcontrib>PIMENTEL, D. R</creatorcontrib><creatorcontrib>COLUCCI, W. 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S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1998-09-29</date><risdate>1998</risdate><volume>98</volume><issue>13</issue><spage>1329</spage><epage>1334</epage><pages>1329-1334</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Myocardial sympathetic activity is increased in heart failure. We tested the hypothesis that norepinephrine (NE) stimulates apoptosis in adult rat ventricular myocytes in vitro.
Myocytes were exposed to NE alone (10 micromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoproterenol (ISO, 10 micromol/L) for 24 hours. NE and ISO decreased the number of viable myocytes by approximately 35%. This effect was completely blocked by the beta-adrenergic antagonist propranolol but was not affected by the alpha1-adrenergic antagonist prazosin. NE increased DNA laddering on agarose gel electrophoresis and increased the percentage of cells that were stained by terminal deoxynucleotidyl transferase-mediated nick end-labeling from 5.8+/-1. 0% to 21.0+/-2.3% (P<0.01; n=4). NE likewise increased the percentage of apoptotic cells with hypodiploid DNA content as assessed by flow cytometry from 7.8+/-0.7% to 16.7+/-2.2% (P<0.01; n=6), and this effect was abolished by propranolol but not prazosin. ISO and forskolin (10 micromol/L) mimicked the effect of NE, increasing the percentage of apoptotic cells to 14.7+/-1.9% and 14. 4+/-2.2%, respectively. NE-stimulated apoptosis was abolished by the protein kinase A inhibitor H-89 (20 micromol/L) or the voltage-dependent calcium channel blockers diltiazem and nifedipine.
NE, acting via the ss-adrenergic pathway, stimulates apoptosis in adult rat cardiac myocytes in vitro. This effect is mediated by protein kinase A and requires calcium entry via voltage-dependent calcium channels. NE-stimulated apoptosis of cardiac myocytes may contribute to the progression of myocardial failure.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9751683</pmid><doi>10.1161/01.CIR.98.13.1329</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 1998-09, Vol.98 (13), p.1329-1334 |
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| language | eng |
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| subjects | Adenylyl Cyclases - physiology Animals Apoptosis - drug effects Biological and medical sciences Calcium Channels - physiology Cardiology. Vascular system Cells, Cultured Cyclic AMP-Dependent Protein Kinases - physiology Flow Cytometry Heart Heart - drug effects Heart failure, cardiogenic pulmonary edema, cardiac enlargement Isoproterenol - pharmacology Male Medical sciences Myocardium - cytology Norepinephrine - pharmacology Rats Rats, Sprague-Dawley Receptors, Adrenergic, beta - drug effects |
| title | Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway |
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