Angiotensin AT1 receptor blockers suppress ischemia/reperfusion-induced gastric injury in rats
Ischemia/reperfusion (I/R) damages gastric mucosa via reactive oxygen species (ROS) activity. ROS was reportedly produced through angiotensin II stimulation in tissues such as kidney, heart and brain. To determine whether AT1 receptor plays a role in gastric mucosal damage, we examined the effect of...
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| Veröffentlicht in: | Inflammopharmacology 2007-08, Vol.15 (4), p.171-174 |
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| creator | Nakagiri, A Sunamoto, M Murakami, M |
| description | Ischemia/reperfusion (I/R) damages gastric mucosa via reactive oxygen species (ROS) activity. ROS was reportedly produced through angiotensin II stimulation in tissues such as kidney, heart and brain. To determine whether AT1 receptor plays a role in gastric mucosal damage, we examined the effect of AT1 receptor blocker (ARB; losartan, candesartan, valsartan) on I/R-induced gastric injury in rats. I/R produced microscopic gastric hemorrhagic injury, and increased gastric microvascular permeability and H(2)O(2) production in rats. The mucosal lesions induced by I/R were attenuated by pretreatment of each ARB. The increase in microvascular permeability was suppressed by losartan pretreatment. Additionally, I/R-caused H(2)O(2) activation was not observed by pretreatment of losartan, candesartan and valsartan. These results suggest that angiotensin II stimulation via AT1 receptor and following ROS production in the stomach contribute to the pathogenesis of the gastric I/R injury. |
| doi_str_mv | 10.1007/s10787-006-1551-3 |
| format | Article |
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ROS was reportedly produced through angiotensin II stimulation in tissues such as kidney, heart and brain. To determine whether AT1 receptor plays a role in gastric mucosal damage, we examined the effect of AT1 receptor blocker (ARB; losartan, candesartan, valsartan) on I/R-induced gastric injury in rats. I/R produced microscopic gastric hemorrhagic injury, and increased gastric microvascular permeability and H(2)O(2) production in rats. The mucosal lesions induced by I/R were attenuated by pretreatment of each ARB. The increase in microvascular permeability was suppressed by losartan pretreatment. Additionally, I/R-caused H(2)O(2) activation was not observed by pretreatment of losartan, candesartan and valsartan. These results suggest that angiotensin II stimulation via AT1 receptor and following ROS production in the stomach contribute to the pathogenesis of the gastric I/R injury.</description><identifier>ISSN: 0925-4692</identifier><identifier>EISSN: 1568-5608</identifier><identifier>DOI: 10.1007/s10787-006-1551-3</identifier><identifier>PMID: 17701020</identifier><language>eng</language><publisher>Switzerland</publisher><subject>Angiotensin II - physiology ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Animals ; Benzimidazoles - pharmacology ; Capillary Permeability - drug effects ; Gastric Mucosa - blood supply ; Gastric Mucosa - drug effects ; Gastric Mucosa - pathology ; Hydrogen Peroxide - metabolism ; Losartan - pharmacology ; Male ; Microcirculation - drug effects ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Reperfusion Injury - prevention & control ; Tetrazoles - pharmacology ; Valine - analogs & derivatives ; Valine - pharmacology ; Valsartan</subject><ispartof>Inflammopharmacology, 2007-08, Vol.15 (4), p.171-174</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c245t-365a9901b3a145a072b742670d8c84fea8714e62b7f5d9c3e3477ad66f7c9d6e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17701020$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakagiri, A</creatorcontrib><creatorcontrib>Sunamoto, M</creatorcontrib><creatorcontrib>Murakami, M</creatorcontrib><title>Angiotensin AT1 receptor blockers suppress ischemia/reperfusion-induced gastric injury in rats</title><title>Inflammopharmacology</title><addtitle>Inflammopharmacology</addtitle><description>Ischemia/reperfusion (I/R) damages gastric mucosa via reactive oxygen species (ROS) activity. ROS was reportedly produced through angiotensin II stimulation in tissues such as kidney, heart and brain. To determine whether AT1 receptor plays a role in gastric mucosal damage, we examined the effect of AT1 receptor blocker (ARB; losartan, candesartan, valsartan) on I/R-induced gastric injury in rats. I/R produced microscopic gastric hemorrhagic injury, and increased gastric microvascular permeability and H(2)O(2) production in rats. The mucosal lesions induced by I/R were attenuated by pretreatment of each ARB. The increase in microvascular permeability was suppressed by losartan pretreatment. Additionally, I/R-caused H(2)O(2) activation was not observed by pretreatment of losartan, candesartan and valsartan. These results suggest that angiotensin II stimulation via AT1 receptor and following ROS production in the stomach contribute to the pathogenesis of the gastric I/R injury.</description><subject>Angiotensin II - physiology</subject><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Animals</subject><subject>Benzimidazoles - pharmacology</subject><subject>Capillary Permeability - drug effects</subject><subject>Gastric Mucosa - blood supply</subject><subject>Gastric Mucosa - drug effects</subject><subject>Gastric Mucosa - pathology</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Losartan - pharmacology</subject><subject>Male</subject><subject>Microcirculation - drug effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Tetrazoles - pharmacology</subject><subject>Valine - analogs & derivatives</subject><subject>Valine - pharmacology</subject><subject>Valsartan</subject><issn>0925-4692</issn><issn>1568-5608</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1PwzAURS0EoqXwA1hQJjbDsx3byVhVfElILGXFcpwXMLRJ8EsG_j2pWomR6UpP5149HcYuBdwIAHtLAmxhOYDhQmvB1RGbC20Krg0Ux2wOpdQ8N6WcsTOiT5hAa8pTNhPWggAJc_a2bN9jN2BLsc2Wa5ElDNgPXcqqTRe-MFFGY98nJMoihQ_cRn-bsMfUjBS7lse2HgPW2bunIcWQxfZzTD9TZMkPdM5OGr8hvDjkgr3e361Xj_z55eFptXzmQeZ64MpoX5YgKuVFrj1YWdlcGgt1EYq8QV9YkaOZro2uy6BQ5db62pjGhrI2qBbser_bp-57RBrcdvoWNxvfYjeSM4UwqpDyX1CCtNpYPYFiD4bUESVsXJ_i1qcfJ8Dt7Lu9fTdJdTv7Tk2dq8P4WG2x_mscdKtfN76AyQ</recordid><startdate>200708</startdate><enddate>200708</enddate><creator>Nakagiri, A</creator><creator>Sunamoto, M</creator><creator>Murakami, M</creator><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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200708</creationdate><title>Angiotensin AT1 receptor blockers suppress ischemia/reperfusion-induced gastric injury in rats</title><author>Nakagiri, A ; Sunamoto, M ; Murakami, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c245t-365a9901b3a145a072b742670d8c84fea8714e62b7f5d9c3e3477ad66f7c9d6e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Angiotensin II - physiology</topic><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Animals</topic><topic>Benzimidazoles - pharmacology</topic><topic>Capillary Permeability - drug effects</topic><topic>Gastric Mucosa - blood supply</topic><topic>Gastric Mucosa - drug effects</topic><topic>Gastric Mucosa - pathology</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Losartan - pharmacology</topic><topic>Male</topic><topic>Microcirculation - drug effects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Tetrazoles - pharmacology</topic><topic>Valine - analogs & derivatives</topic><topic>Valine - pharmacology</topic><topic>Valsartan</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakagiri, A</creatorcontrib><creatorcontrib>Sunamoto, M</creatorcontrib><creatorcontrib>Murakami, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakagiri, A</au><au>Sunamoto, M</au><au>Murakami, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin AT1 receptor blockers suppress ischemia/reperfusion-induced gastric injury in rats</atitle><jtitle>Inflammopharmacology</jtitle><addtitle>Inflammopharmacology</addtitle><date>2007-08</date><risdate>2007</risdate><volume>15</volume><issue>4</issue><spage>171</spage><epage>174</epage><pages>171-174</pages><issn>0925-4692</issn><eissn>1568-5608</eissn><abstract>Ischemia/reperfusion (I/R) damages gastric mucosa via reactive oxygen species (ROS) activity. ROS was reportedly produced through angiotensin II stimulation in tissues such as kidney, heart and brain. To determine whether AT1 receptor plays a role in gastric mucosal damage, we examined the effect of AT1 receptor blocker (ARB; losartan, candesartan, valsartan) on I/R-induced gastric injury in rats. I/R produced microscopic gastric hemorrhagic injury, and increased gastric microvascular permeability and H(2)O(2) production in rats. The mucosal lesions induced by I/R were attenuated by pretreatment of each ARB. The increase in microvascular permeability was suppressed by losartan pretreatment. Additionally, I/R-caused H(2)O(2) activation was not observed by pretreatment of losartan, candesartan and valsartan. These results suggest that angiotensin II stimulation via AT1 receptor and following ROS production in the stomach contribute to the pathogenesis of the gastric I/R injury.</abstract><cop>Switzerland</cop><pmid>17701020</pmid><doi>10.1007/s10787-006-1551-3</doi><tpages>4</tpages></addata></record> |
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| subjects | Angiotensin II - physiology Angiotensin II Type 1 Receptor Blockers - pharmacology Animals Benzimidazoles - pharmacology Capillary Permeability - drug effects Gastric Mucosa - blood supply Gastric Mucosa - drug effects Gastric Mucosa - pathology Hydrogen Peroxide - metabolism Losartan - pharmacology Male Microcirculation - drug effects Rats Rats, Sprague-Dawley Reperfusion Injury - metabolism Reperfusion Injury - pathology Reperfusion Injury - prevention & control Tetrazoles - pharmacology Valine - analogs & derivatives Valine - pharmacology Valsartan |
| title | Angiotensin AT1 receptor blockers suppress ischemia/reperfusion-induced gastric injury in rats |
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