Loading…

Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmune myocarditis

Excess amount of cytokine produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Some angiotensin II receptor type 1 antagonists are reported to inhibit proinflammatory cytokine production in vitro and in vivo. We tested the hypothesis that olmesartan, a...

Full description

Saved in:
Bibliographic Details
Published in:Molecular and cellular biochemistry 2004-04, Vol.259 (1-2), p.217-222
Main Authors: Nimata, Masaomi, Kishimoto, Chiharu, Yuan, Zuyi, Shioji, Keisuke
Format: Article
Language:English
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 222
container_issue 1-2
container_start_page 217
container_title Molecular and cellular biochemistry
container_volume 259
creator Nimata, Masaomi
Kishimoto, Chiharu
Yuan, Zuyi
Shioji, Keisuke
description Excess amount of cytokine produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Some angiotensin II receptor type 1 antagonists are reported to inhibit proinflammatory cytokine production in vitro and in vivo. We tested the hypothesis that olmesartan, a novel angiotensin II receptor type 1 antagonist, ameliorated experimental autoimmune myocarditis (EAM) in rats attributing to the suppression of inflammatory cytokines in the heart. We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The results showed that olmesartan decreased blood pressure significantly compared with the untreated group, but markedly reduced the severity of myocarditis by comparing the heart weight/body weight ratio, pericardial effusion scores, macroscopic scores and microscopic scores. Myocardial interleukin (IL)- 1beta expression by western blotting and IL-1beta-positive staining cells by immunohistochemistry were significantly lower in rats with EAM given olmesartan treatment compared with those of rats given vehicle. We conclude that Olmesartan ameliorates acute EAM in rats. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications.
doi_str_mv 10.1023/B:MCBI.0000021379.82282.53
format article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_1464505927</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1464505927</sourcerecordid><originalsourceid>FETCH-LOGICAL-p267t-6f0c4762e7b4e527e81f8ad83b96c0347a618a0a7052763dd7b90d3e682f3cd63</originalsourceid><addsrcrecordid>eNpdkF1LwzAYhYMobk7_goRdebHWfLRJ6p0bfgwm3uh1ydK3I6NNapMO9u-tOG98OfBenIfD4SA0pySlhPH75cPbarlOyc8xymWRKsYUS3N-hqY0lzzJClqcoynhhCSKSjlBVyHsCaGj6CWa0JyyrGByig5LcFBbY3WDoa7BxIB9jX3TQtB91G6BNXb-AA3Wbmd9BBesw-s17sFAF32P47EDTEc76p13NsQFHjrvsDZDBKyH6G3bDg5we_RG95WNNlyji1o3AW5Of4Y-n58-Vq_J5v1lvXrcJB0TMiaiJiaTgoHcZpAzCYrWSleKbwthCM-kFlRpoiUZTcGrSm4LUnEQitXcVILP0N1vbtf7rwFCLFsbDDSNduCHUNJMZDnJxylGdP4P3fuhd2O7UuaCUZqpfIRuT9CwbaEqu962uj-Wf4Pyb2McekI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>756211485</pqid></control><display><type>article</type><title>Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmune myocarditis</title><source>Springer Nature</source><creator>Nimata, Masaomi ; Kishimoto, Chiharu ; Yuan, Zuyi ; Shioji, Keisuke</creator><creatorcontrib>Nimata, Masaomi ; Kishimoto, Chiharu ; Yuan, Zuyi ; Shioji, Keisuke</creatorcontrib><description>Excess amount of cytokine produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Some angiotensin II receptor type 1 antagonists are reported to inhibit proinflammatory cytokine production in vitro and in vivo. We tested the hypothesis that olmesartan, a novel angiotensin II receptor type 1 antagonist, ameliorated experimental autoimmune myocarditis (EAM) in rats attributing to the suppression of inflammatory cytokines in the heart. We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The results showed that olmesartan decreased blood pressure significantly compared with the untreated group, but markedly reduced the severity of myocarditis by comparing the heart weight/body weight ratio, pericardial effusion scores, macroscopic scores and microscopic scores. Myocardial interleukin (IL)- 1beta expression by western blotting and IL-1beta-positive staining cells by immunohistochemistry were significantly lower in rats with EAM given olmesartan treatment compared with those of rats given vehicle. We conclude that Olmesartan ameliorates acute EAM in rats. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1023/B:MCBI.0000021379.82282.53</identifier><identifier>PMID: 15124927</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Administration, Oral ; Angiotensin II receptors ; Angiotensin II Type 1 Receptor Blockers - administration &amp; dosage ; Animals ; Antihypertensive Agents - administration &amp; dosage ; Autoimmune Diseases - chemically induced ; Autoimmune Diseases - immunology ; Blood pressure ; Body weight ; Cytokines ; Dose-Response Relationship, Drug ; Female ; Imidazoles - administration &amp; dosage ; Interleukin-1 - biosynthesis ; Male ; Myocarditis - chemically induced ; Myocarditis - drug therapy ; Myocarditis - immunology ; Myocarditis - metabolism ; Myocarditis - pathology ; Myocardium - metabolism ; Myocardium - pathology ; Myosins - administration &amp; dosage ; Myosins - immunology ; Olmesartan Medoxomil ; Rats ; Rats, Inbred Lew ; Receptor, Angiotensin, Type 1 - immunology ; Rodents ; Swine ; Tetrazoles - administration &amp; dosage</subject><ispartof>Molecular and cellular biochemistry, 2004-04, Vol.259 (1-2), p.217-222</ispartof><rights>Kluwer Academic Publishers 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15124927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nimata, Masaomi</creatorcontrib><creatorcontrib>Kishimoto, Chiharu</creatorcontrib><creatorcontrib>Yuan, Zuyi</creatorcontrib><creatorcontrib>Shioji, Keisuke</creatorcontrib><title>Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmune myocarditis</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>Excess amount of cytokine produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Some angiotensin II receptor type 1 antagonists are reported to inhibit proinflammatory cytokine production in vitro and in vivo. We tested the hypothesis that olmesartan, a novel angiotensin II receptor type 1 antagonist, ameliorated experimental autoimmune myocarditis (EAM) in rats attributing to the suppression of inflammatory cytokines in the heart. We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The results showed that olmesartan decreased blood pressure significantly compared with the untreated group, but markedly reduced the severity of myocarditis by comparing the heart weight/body weight ratio, pericardial effusion scores, macroscopic scores and microscopic scores. Myocardial interleukin (IL)- 1beta expression by western blotting and IL-1beta-positive staining cells by immunohistochemistry were significantly lower in rats with EAM given olmesartan treatment compared with those of rats given vehicle. We conclude that Olmesartan ameliorates acute EAM in rats. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications.</description><subject>Administration, Oral</subject><subject>Angiotensin II receptors</subject><subject>Angiotensin II Type 1 Receptor Blockers - administration &amp; dosage</subject><subject>Animals</subject><subject>Antihypertensive Agents - administration &amp; dosage</subject><subject>Autoimmune Diseases - chemically induced</subject><subject>Autoimmune Diseases - immunology</subject><subject>Blood pressure</subject><subject>Body weight</subject><subject>Cytokines</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Imidazoles - administration &amp; dosage</subject><subject>Interleukin-1 - biosynthesis</subject><subject>Male</subject><subject>Myocarditis - chemically induced</subject><subject>Myocarditis - drug therapy</subject><subject>Myocarditis - immunology</subject><subject>Myocarditis - metabolism</subject><subject>Myocarditis - pathology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myosins - administration &amp; dosage</subject><subject>Myosins - immunology</subject><subject>Olmesartan Medoxomil</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Receptor, Angiotensin, Type 1 - immunology</subject><subject>Rodents</subject><subject>Swine</subject><subject>Tetrazoles - administration &amp; dosage</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNpdkF1LwzAYhYMobk7_goRdebHWfLRJ6p0bfgwm3uh1ydK3I6NNapMO9u-tOG98OfBenIfD4SA0pySlhPH75cPbarlOyc8xymWRKsYUS3N-hqY0lzzJClqcoynhhCSKSjlBVyHsCaGj6CWa0JyyrGByig5LcFBbY3WDoa7BxIB9jX3TQtB91G6BNXb-AA3Wbmd9BBesw-s17sFAF32P47EDTEc76p13NsQFHjrvsDZDBKyH6G3bDg5we_RG95WNNlyji1o3AW5Of4Y-n58-Vq_J5v1lvXrcJB0TMiaiJiaTgoHcZpAzCYrWSleKbwthCM-kFlRpoiUZTcGrSm4LUnEQitXcVILP0N1vbtf7rwFCLFsbDDSNduCHUNJMZDnJxylGdP4P3fuhd2O7UuaCUZqpfIRuT9CwbaEqu962uj-Wf4Pyb2McekI</recordid><startdate>200404</startdate><enddate>200404</enddate><creator>Nimata, Masaomi</creator><creator>Kishimoto, Chiharu</creator><creator>Yuan, Zuyi</creator><creator>Shioji, Keisuke</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>200404</creationdate><title>Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmune myocarditis</title><author>Nimata, Masaomi ; Kishimoto, Chiharu ; Yuan, Zuyi ; Shioji, Keisuke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p267t-6f0c4762e7b4e527e81f8ad83b96c0347a618a0a7052763dd7b90d3e682f3cd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Administration, Oral</topic><topic>Angiotensin II receptors</topic><topic>Angiotensin II Type 1 Receptor Blockers - administration &amp; dosage</topic><topic>Animals</topic><topic>Antihypertensive Agents - administration &amp; dosage</topic><topic>Autoimmune Diseases - chemically induced</topic><topic>Autoimmune Diseases - immunology</topic><topic>Blood pressure</topic><topic>Body weight</topic><topic>Cytokines</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>Imidazoles - administration &amp; dosage</topic><topic>Interleukin-1 - biosynthesis</topic><topic>Male</topic><topic>Myocarditis - chemically induced</topic><topic>Myocarditis - drug therapy</topic><topic>Myocarditis - immunology</topic><topic>Myocarditis - metabolism</topic><topic>Myocarditis - pathology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Myosins - administration &amp; dosage</topic><topic>Myosins - immunology</topic><topic>Olmesartan Medoxomil</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Receptor, Angiotensin, Type 1 - immunology</topic><topic>Rodents</topic><topic>Swine</topic><topic>Tetrazoles - administration &amp; dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nimata, Masaomi</creatorcontrib><creatorcontrib>Kishimoto, Chiharu</creatorcontrib><creatorcontrib>Yuan, Zuyi</creatorcontrib><creatorcontrib>Shioji, Keisuke</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest_Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Science Database (ProQuest)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nimata, Masaomi</au><au>Kishimoto, Chiharu</au><au>Yuan, Zuyi</au><au>Shioji, Keisuke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmune myocarditis</atitle><jtitle>Molecular and cellular biochemistry</jtitle><addtitle>Mol Cell Biochem</addtitle><date>2004-04</date><risdate>2004</risdate><volume>259</volume><issue>1-2</issue><spage>217</spage><epage>222</epage><pages>217-222</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Excess amount of cytokine produced by inflammatory stimuli contributes to the progression of myocardial damage in myocarditis. Some angiotensin II receptor type 1 antagonists are reported to inhibit proinflammatory cytokine production in vitro and in vivo. We tested the hypothesis that olmesartan, a novel angiotensin II receptor type 1 antagonist, ameliorated experimental autoimmune myocarditis (EAM) in rats attributing to the suppression of inflammatory cytokines in the heart. We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The results showed that olmesartan decreased blood pressure significantly compared with the untreated group, but markedly reduced the severity of myocarditis by comparing the heart weight/body weight ratio, pericardial effusion scores, macroscopic scores and microscopic scores. Myocardial interleukin (IL)- 1beta expression by western blotting and IL-1beta-positive staining cells by immunohistochemistry were significantly lower in rats with EAM given olmesartan treatment compared with those of rats given vehicle. We conclude that Olmesartan ameliorates acute EAM in rats. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>15124927</pmid><doi>10.1023/B:MCBI.0000021379.82282.53</doi><tpages>6</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0300-8177
ispartof Molecular and cellular biochemistry, 2004-04, Vol.259 (1-2), p.217-222
issn 0300-8177
1573-4919
language eng
recordid cdi_proquest_miscellaneous_1464505927
source Springer Nature
subjects Administration, Oral
Angiotensin II receptors
Angiotensin II Type 1 Receptor Blockers - administration & dosage
Animals
Antihypertensive Agents - administration & dosage
Autoimmune Diseases - chemically induced
Autoimmune Diseases - immunology
Blood pressure
Body weight
Cytokines
Dose-Response Relationship, Drug
Female
Imidazoles - administration & dosage
Interleukin-1 - biosynthesis
Male
Myocarditis - chemically induced
Myocarditis - drug therapy
Myocarditis - immunology
Myocarditis - metabolism
Myocarditis - pathology
Myocardium - metabolism
Myocardium - pathology
Myosins - administration & dosage
Myosins - immunology
Olmesartan Medoxomil
Rats
Rats, Inbred Lew
Receptor, Angiotensin, Type 1 - immunology
Rodents
Swine
Tetrazoles - administration & dosage
title Beneficial effects of olmesartan, a novel angiotensin II receptor type 1 antagonist, upon acute autoimmune myocarditis
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T02%3A53%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Beneficial%20effects%20of%20olmesartan,%20a%20novel%20angiotensin%20II%20receptor%20type%201%20antagonist,%20upon%20acute%20autoimmune%20myocarditis&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Nimata,%20Masaomi&rft.date=2004-04&rft.volume=259&rft.issue=1-2&rft.spage=217&rft.epage=222&rft.pages=217-222&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1023/B:MCBI.0000021379.82282.53&rft_dat=%3Cproquest_pubme%3E1464505927%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-p267t-6f0c4762e7b4e527e81f8ad83b96c0347a618a0a7052763dd7b90d3e682f3cd63%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=756211485&rft_id=info:pmid/15124927&rfr_iscdi=true