Angiotensin-Converting Enzyme Inhibition and Salt in Experimental Myocardial Infarction
It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. In this study, to determine whether...
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Veröffentlicht in: | Journal of cardiovascular pharmacology 1998-09, Vol.32 (3), p.357-365 |
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creator | Yoshida, Kazunori Kohzuki, Masahiro Casley, David J Johnston, Colin I |
description | It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. In this study, to determine whether the beneficial effects of angiotensin-converting enzyme inhibition on cardiac hypertrophy after myocardial infarction are due to a reduction in ventricular afterload or to inhibition of cardiac angiotensin-converting enzyme, we used sodium loading during angiotensin-converting enzyme inhibition. The rat model of myocardial infarction was treated with a vehicle, 1% saline, as drinking fluid, perindopril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevented cardiac hypertrophy, and inhibited cardiac angiotensin-converting enzyme. The effects of perindopril on blood pressure and cardiac hypertrophy were abolished by sodium loading, which did not alter the degree of cardiac angiotensin-converting enzyme inhibition. Thus the actions of perindopril on cardiac hypertrophy depend more on blood pressure reduction than on cardiac angiotensin-converting enzyme inhibition in the rat model of myocardial infarction. |
doi_str_mv | 10.1097/00005344-199809000-00004 |
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In this study, to determine whether the beneficial effects of angiotensin-converting enzyme inhibition on cardiac hypertrophy after myocardial infarction are due to a reduction in ventricular afterload or to inhibition of cardiac angiotensin-converting enzyme, we used sodium loading during angiotensin-converting enzyme inhibition. The rat model of myocardial infarction was treated with a vehicle, 1% saline, as drinking fluid, perindopril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevented cardiac hypertrophy, and inhibited cardiac angiotensin-converting enzyme. The effects of perindopril on blood pressure and cardiac hypertrophy were abolished by sodium loading, which did not alter the degree of cardiac angiotensin-converting enzyme inhibition. Thus the actions of perindopril on cardiac hypertrophy depend more on blood pressure reduction than on cardiac angiotensin-converting enzyme inhibition in the rat model of myocardial infarction.</description><identifier>ISSN: 0160-2446</identifier><identifier>EISSN: 1533-4023</identifier><identifier>DOI: 10.1097/00005344-199809000-00004</identifier><identifier>PMID: 9733347</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins, Inc</publisher><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Animals ; Autoradiography ; Binding Sites ; Blood Pressure - drug effects ; Cardiomegaly - prevention & control ; Indoles - therapeutic use ; Male ; Myocardial Infarction - drug therapy ; Peptidyl-Dipeptidase A - metabolism ; Perindopril ; Rats ; Rats, Sprague-Dawley ; Renin - blood ; Sodium Chloride, Dietary - administration & dosage</subject><ispartof>Journal of cardiovascular pharmacology, 1998-09, Vol.32 (3), p.357-365</ispartof><rights>1998 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00005344-199809000-00004$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>314,780,784,4607,27923,27924,65232</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9733347$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshida, Kazunori</creatorcontrib><creatorcontrib>Kohzuki, Masahiro</creatorcontrib><creatorcontrib>Casley, David J</creatorcontrib><creatorcontrib>Johnston, Colin I</creatorcontrib><title>Angiotensin-Converting Enzyme Inhibition and Salt in Experimental Myocardial Infarction</title><title>Journal of cardiovascular pharmacology</title><addtitle>J Cardiovasc Pharmacol</addtitle><description>It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. In this study, to determine whether the beneficial effects of angiotensin-converting enzyme inhibition on cardiac hypertrophy after myocardial infarction are due to a reduction in ventricular afterload or to inhibition of cardiac angiotensin-converting enzyme, we used sodium loading during angiotensin-converting enzyme inhibition. The rat model of myocardial infarction was treated with a vehicle, 1% saline, as drinking fluid, perindopril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevented cardiac hypertrophy, and inhibited cardiac angiotensin-converting enzyme. The effects of perindopril on blood pressure and cardiac hypertrophy were abolished by sodium loading, which did not alter the degree of cardiac angiotensin-converting enzyme inhibition. Thus the actions of perindopril on cardiac hypertrophy depend more on blood pressure reduction than on cardiac angiotensin-converting enzyme inhibition in the rat model of myocardial infarction.</description><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Animals</subject><subject>Autoradiography</subject><subject>Binding Sites</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiomegaly - prevention & control</subject><subject>Indoles - therapeutic use</subject><subject>Male</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Peptidyl-Dipeptidase A - metabolism</subject><subject>Perindopril</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renin - blood</subject><subject>Sodium Chloride, Dietary - administration & dosage</subject><issn>0160-2446</issn><issn>1533-4023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1UMtOwzAQtBColMInIPnELWBnHT-OVVWgUhEHQBwjJ3FaQ-IEO6WUr8dVe2Uu-5jRanYQwpTcUqLEHYnIgLGEKiWJilOyX7ETNKYZQMJICqdoTCgnScoYP0cXIXwQQlkm-AiNlAAAJsbofepWthuMC9Yls859Gz9Yt8Jz97trDV64tS3sYDuHtavwi24GbB2e__TG29a4QTf4adeV2lc2tgtXa1_u5ZforNZNMFfHOkFv9_PX2WOyfH5YzKbLpKcSWFKplHADSmml60JUxESDwCUnLC0jUlkLINJAllEtCwANopSs4IRzQqSCCbo53O1997UxYchbG0rTNNqZbhNyAVKxg_D6KNwUranyPvrXfpcfk4g8O_DbrhmMD5_NZmt8vjbx5XX-X97wBzDncM8</recordid><startdate>199809</startdate><enddate>199809</enddate><creator>Yoshida, Kazunori</creator><creator>Kohzuki, Masahiro</creator><creator>Casley, David J</creator><creator>Johnston, Colin I</creator><general>Lippincott Williams & Wilkins, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>199809</creationdate><title>Angiotensin-Converting Enzyme Inhibition and Salt in Experimental Myocardial Infarction</title><author>Yoshida, Kazunori ; Kohzuki, Masahiro ; Casley, David J ; Johnston, Colin I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1834-d9206e399a9afb7d0e4573686042cccc28f7308e3551a8b33a37c84b606600893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</topic><topic>Animals</topic><topic>Autoradiography</topic><topic>Binding Sites</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiomegaly - prevention & control</topic><topic>Indoles - therapeutic use</topic><topic>Male</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Peptidyl-Dipeptidase A - metabolism</topic><topic>Perindopril</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renin - blood</topic><topic>Sodium Chloride, Dietary - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshida, Kazunori</creatorcontrib><creatorcontrib>Kohzuki, Masahiro</creatorcontrib><creatorcontrib>Casley, David J</creatorcontrib><creatorcontrib>Johnston, Colin I</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cardiovascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshida, Kazunori</au><au>Kohzuki, Masahiro</au><au>Casley, David J</au><au>Johnston, Colin I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin-Converting Enzyme Inhibition and Salt in Experimental Myocardial Infarction</atitle><jtitle>Journal of cardiovascular pharmacology</jtitle><addtitle>J Cardiovasc Pharmacol</addtitle><date>1998-09</date><risdate>1998</risdate><volume>32</volume><issue>3</issue><spage>357</spage><epage>365</epage><pages>357-365</pages><issn>0160-2446</issn><eissn>1533-4023</eissn><abstract>It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. In this study, to determine whether the beneficial effects of angiotensin-converting enzyme inhibition on cardiac hypertrophy after myocardial infarction are due to a reduction in ventricular afterload or to inhibition of cardiac angiotensin-converting enzyme, we used sodium loading during angiotensin-converting enzyme inhibition. The rat model of myocardial infarction was treated with a vehicle, 1% saline, as drinking fluid, perindopril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevented cardiac hypertrophy, and inhibited cardiac angiotensin-converting enzyme. The effects of perindopril on blood pressure and cardiac hypertrophy were abolished by sodium loading, which did not alter the degree of cardiac angiotensin-converting enzyme inhibition. Thus the actions of perindopril on cardiac hypertrophy depend more on blood pressure reduction than on cardiac angiotensin-converting enzyme inhibition in the rat model of myocardial infarction.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>9733347</pmid><doi>10.1097/00005344-199809000-00004</doi><tpages>9</tpages></addata></record> |
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subjects | Angiotensin-Converting Enzyme Inhibitors - therapeutic use Animals Autoradiography Binding Sites Blood Pressure - drug effects Cardiomegaly - prevention & control Indoles - therapeutic use Male Myocardial Infarction - drug therapy Peptidyl-Dipeptidase A - metabolism Perindopril Rats Rats, Sprague-Dawley Renin - blood Sodium Chloride, Dietary - administration & dosage |
title | Angiotensin-Converting Enzyme Inhibition and Salt in Experimental Myocardial Infarction |
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