Role of Atrial Natriuretic Peptide in Oxytocin Induced Cardioprotection
Background The purpose of this study was to determine whether endogenous atrial natriuretic peptide (ANP) contributes to the protective effect of neurohypophysial hormone oxytocin (OT) in heart preconditioning. Methods Sprague–Dawley male rats were subjected to 25 min regional ischaemia and 120 min...
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description | Background The purpose of this study was to determine whether endogenous atrial natriuretic peptide (ANP) contributes to the protective effect of neurohypophysial hormone oxytocin (OT) in heart preconditioning. Methods Sprague–Dawley male rats were subjected to 25 min regional ischaemia and 120 min reperfusion and were divided into eight groups. Oxytocin or an equivalent volume of saline was administrated intraperitoneally, 30 min before ischaemia. The OT receptor antagonist (atosiban), ANP receptor antagonist (anantin) and nitric oxide synthase inhibitor (L-NAME) were injected 10 min before OT. In other groups, atosiban, anantin and L-NAME were only administered 40 min prior to ischaemia. Results Compared with the ischaemia/reperfusion group (I/R), alterations in infarct size, biochemical parameters [LDH (lactate dehydrogenase), CK-MB (creatine kinase-MB), MDA (malondialdehyde) plasma levels] and severity of ventricular arrhythmia due to I/R injury were attenuated and VF was abolished by OT treatment. These OT effects were eliminated by OT and ANP receptor blockers and nitric oxide synthase inhibitor , but anantin did not reverse the effect of OT in lipid peroxidation. Conclusions These findings demonstrate an important contributory role of ANP in the OT induced protection in myocardial ischaemia reperfusion. OT also reduced lipid peroxidation with a NO-dependent mechanism. |
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Methods Sprague–Dawley male rats were subjected to 25 min regional ischaemia and 120 min reperfusion and were divided into eight groups. Oxytocin or an equivalent volume of saline was administrated intraperitoneally, 30 min before ischaemia. The OT receptor antagonist (atosiban), ANP receptor antagonist (anantin) and nitric oxide synthase inhibitor (L-NAME) were injected 10 min before OT. In other groups, atosiban, anantin and L-NAME were only administered 40 min prior to ischaemia. Results Compared with the ischaemia/reperfusion group (I/R), alterations in infarct size, biochemical parameters [LDH (lactate dehydrogenase), CK-MB (creatine kinase-MB), MDA (malondialdehyde) plasma levels] and severity of ventricular arrhythmia due to I/R injury were attenuated and VF was abolished by OT treatment. These OT effects were eliminated by OT and ANP receptor blockers and nitric oxide synthase inhibitor , but anantin did not reverse the effect of OT in lipid peroxidation. Conclusions These findings demonstrate an important contributory role of ANP in the OT induced protection in myocardial ischaemia reperfusion. OT also reduced lipid peroxidation with a NO-dependent mechanism.</description><identifier>ISSN: 1443-9506</identifier><identifier>EISSN: 1444-2892</identifier><identifier>DOI: 10.1016/j.hlc.2014.05.023</identifier><identifier>PMID: 25126708</identifier><language>eng</language><publisher>Australia: Elsevier B.V</publisher><subject>Animals ; Atrial Natriuretic Factor - metabolism ; Atrial natriuretic peptide ; Cardiotonic Agents - pharmacology ; Cardiovascular ; Enzyme Inhibitors - pharmacology ; Hormone Antagonists - pharmacology ; Ischaemia reperfusion ; Lipid Peroxidation - drug effects ; Male ; Myocardial Infarction - metabolism ; Myocardial Infarction - prevention & control ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - prevention & control ; NG-Nitroarginine Methyl Ester - pharmacology ; Oxidative stress ; Oxytocics - pharmacology ; Oxytocin ; Oxytocin - pharmacology ; Peptides, Cyclic - pharmacology ; Preconditioning ; Rats ; Rats, Sprague-Dawley ; Vasotocin - analogs & derivatives ; Vasotocin - pharmacology</subject><ispartof>Heart, lung & circulation, 2015-01, Vol.24 (1), p.86-93</ispartof><rights>Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ)</rights><rights>2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ)</rights><rights>Copyright © 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c587t-5a91dac566f86fd34f9e3b925de18559771ae8bbe1bfab6cbb20f01bcb1704853</citedby><cites>FETCH-LOGICAL-c587t-5a91dac566f86fd34f9e3b925de18559771ae8bbe1bfab6cbb20f01bcb1704853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.hlc.2014.05.023$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25126708$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Houshmand, Fariba, PhD</creatorcontrib><creatorcontrib>Faghihi, Mahdieh, PhD</creatorcontrib><creatorcontrib>Zahediasl, Saleh, PhD</creatorcontrib><title>Role of Atrial Natriuretic Peptide in Oxytocin Induced Cardioprotection</title><title>Heart, lung & circulation</title><addtitle>Heart Lung Circ</addtitle><description>Background The purpose of this study was to determine whether endogenous atrial natriuretic peptide (ANP) contributes to the protective effect of neurohypophysial hormone oxytocin (OT) in heart preconditioning. Methods Sprague–Dawley male rats were subjected to 25 min regional ischaemia and 120 min reperfusion and were divided into eight groups. Oxytocin or an equivalent volume of saline was administrated intraperitoneally, 30 min before ischaemia. The OT receptor antagonist (atosiban), ANP receptor antagonist (anantin) and nitric oxide synthase inhibitor (L-NAME) were injected 10 min before OT. In other groups, atosiban, anantin and L-NAME were only administered 40 min prior to ischaemia. Results Compared with the ischaemia/reperfusion group (I/R), alterations in infarct size, biochemical parameters [LDH (lactate dehydrogenase), CK-MB (creatine kinase-MB), MDA (malondialdehyde) plasma levels] and severity of ventricular arrhythmia due to I/R injury were attenuated and VF was abolished by OT treatment. These OT effects were eliminated by OT and ANP receptor blockers and nitric oxide synthase inhibitor , but anantin did not reverse the effect of OT in lipid peroxidation. Conclusions These findings demonstrate an important contributory role of ANP in the OT induced protection in myocardial ischaemia reperfusion. OT also reduced lipid peroxidation with a NO-dependent mechanism.</description><subject>Animals</subject><subject>Atrial Natriuretic Factor - metabolism</subject><subject>Atrial natriuretic peptide</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cardiovascular</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Hormone Antagonists - pharmacology</subject><subject>Ischaemia reperfusion</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - prevention & control</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Oxidative stress</subject><subject>Oxytocics - pharmacology</subject><subject>Oxytocin</subject><subject>Oxytocin - pharmacology</subject><subject>Peptides, Cyclic - pharmacology</subject><subject>Preconditioning</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Vasotocin - analogs & derivatives</subject><subject>Vasotocin - pharmacology</subject><issn>1443-9506</issn><issn>1444-2892</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtvFDEQhC0EIiHwA7igOXKZwe3njJCQohWESBFBPM6WHz3Cy-x4sWci9t_jZQMHDpy6D1XV6q8IeQ60Awrq1bb7NvmOURAdlR1l_AE5ByFEy_qBPfy983aQVJ2RJ6VsKQUt-PCYnDEJTGnan5OrT2nCJo3N5ZKjnZoPts414xJ98xH3SwzYxLm5_XlYkq_L9RxWj6HZ2Bxi2ue0oF9imp-SR6OdCj67nxfk67u3Xzbv25vbq-vN5U3rZa-XVtoBgvVSqbFXY-BiHJC7gcmA0Es5aA0We-cQ3Gid8s4xOlJw3oGmopf8grw85dbTP1Ysi9nF4nGa7IxpLQYUF5opoXWVwknqcyol42j2Oe5sPhig5sjPbE3lZ478DJWm8queF_fxq9th-Ov4A6wKXp8EWJ-8i5hN8RHniiTmSsKEFP8b_-Yft5_iHL2dvuMByzatea70DJjCDDWfjwUe-wNBqeQw8F9ibpVi</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Houshmand, Fariba, PhD</creator><creator>Faghihi, Mahdieh, PhD</creator><creator>Zahediasl, Saleh, PhD</creator><general>Elsevier 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>7X8</scope></search><sort><creationdate>20150101</creationdate><title>Role of Atrial Natriuretic Peptide in Oxytocin Induced Cardioprotection</title><author>Houshmand, Fariba, PhD ; Faghihi, Mahdieh, PhD ; Zahediasl, Saleh, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c587t-5a91dac566f86fd34f9e3b925de18559771ae8bbe1bfab6cbb20f01bcb1704853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Atrial Natriuretic Factor - metabolism</topic><topic>Atrial natriuretic peptide</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cardiovascular</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Hormone Antagonists - pharmacology</topic><topic>Ischaemia reperfusion</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - prevention & control</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Oxidative stress</topic><topic>Oxytocics - pharmacology</topic><topic>Oxytocin</topic><topic>Oxytocin - pharmacology</topic><topic>Peptides, Cyclic - pharmacology</topic><topic>Preconditioning</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Vasotocin - analogs & derivatives</topic><topic>Vasotocin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Houshmand, Fariba, PhD</creatorcontrib><creatorcontrib>Faghihi, Mahdieh, PhD</creatorcontrib><creatorcontrib>Zahediasl, Saleh, PhD</creatorcontrib><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>Heart, lung & circulation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Houshmand, Fariba, PhD</au><au>Faghihi, Mahdieh, PhD</au><au>Zahediasl, Saleh, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Atrial Natriuretic Peptide in Oxytocin Induced Cardioprotection</atitle><jtitle>Heart, lung & circulation</jtitle><addtitle>Heart Lung Circ</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>24</volume><issue>1</issue><spage>86</spage><epage>93</epage><pages>86-93</pages><issn>1443-9506</issn><eissn>1444-2892</eissn><abstract>Background The purpose of this study was to determine whether endogenous atrial natriuretic peptide (ANP) contributes to the protective effect of neurohypophysial hormone oxytocin (OT) in heart preconditioning. Methods Sprague–Dawley male rats were subjected to 25 min regional ischaemia and 120 min reperfusion and were divided into eight groups. Oxytocin or an equivalent volume of saline was administrated intraperitoneally, 30 min before ischaemia. The OT receptor antagonist (atosiban), ANP receptor antagonist (anantin) and nitric oxide synthase inhibitor (L-NAME) were injected 10 min before OT. In other groups, atosiban, anantin and L-NAME were only administered 40 min prior to ischaemia. Results Compared with the ischaemia/reperfusion group (I/R), alterations in infarct size, biochemical parameters [LDH (lactate dehydrogenase), CK-MB (creatine kinase-MB), MDA (malondialdehyde) plasma levels] and severity of ventricular arrhythmia due to I/R injury were attenuated and VF was abolished by OT treatment. These OT effects were eliminated by OT and ANP receptor blockers and nitric oxide synthase inhibitor , but anantin did not reverse the effect of OT in lipid peroxidation. Conclusions These findings demonstrate an important contributory role of ANP in the OT induced protection in myocardial ischaemia reperfusion. OT also reduced lipid peroxidation with a NO-dependent mechanism.</abstract><cop>Australia</cop><pub>Elsevier B.V</pub><pmid>25126708</pmid><doi>10.1016/j.hlc.2014.05.023</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Atrial Natriuretic Factor - metabolism Atrial natriuretic peptide Cardiotonic Agents - pharmacology Cardiovascular Enzyme Inhibitors - pharmacology Hormone Antagonists - pharmacology Ischaemia reperfusion Lipid Peroxidation - drug effects Male Myocardial Infarction - metabolism Myocardial Infarction - prevention & control Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - prevention & control NG-Nitroarginine Methyl Ester - pharmacology Oxidative stress Oxytocics - pharmacology Oxytocin Oxytocin - pharmacology Peptides, Cyclic - pharmacology Preconditioning Rats Rats, Sprague-Dawley Vasotocin - analogs & derivatives Vasotocin - pharmacology |
title | Role of Atrial Natriuretic Peptide in Oxytocin Induced Cardioprotection |
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