Effect of Angiotensin II Type 1 Receptor Blockade on Conduit Artery Tone in Subtotally Nephrectomized Rats
Background: Angiotensin II type 1 (AT 1 ) receptor antagonists provide end-organ protection and enhance resistance artery relaxation in uremia. The effect of AT 1 blockade on conduit artery function in renal failure is unknown. Methods: The influence of 8-week losartan therapy (20 mg/kg/day) on tone...
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| Veröffentlicht in: | Nephron 2004-03, Vol.96 (3), p.p91-p98 |
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| creator | Kööbi, Peeter Jolma, Pasi Kalliovalkama, Jarkko Tikkanen, Ilkka Fan, Meng Kähönen, Mika Moilanen, Eeva Pörsti, Ilkka |
| description | Background: Angiotensin II type 1 (AT 1 ) receptor antagonists provide end-organ protection and enhance resistance artery relaxation in uremia. The effect of AT 1 blockade on conduit artery function in renal failure is unknown. Methods: The influence of 8-week losartan therapy (20 mg/kg/day) on tone of isolated main branch mesenteric arterial rings was studied in 5/6 nephrectomized (NX) rats. Blood and urine chemistry were examined, and AT 1 receptors quantified using autoradiography. Results: NX rats showed decreased creatinine clearance without change in blood pressure. Losartan did not influence these variables, although [ 125 I]-Sar1,Ile8-angiotensin II binding to renal AT 1 receptors was significantly prevented. Vasoconstriction to endothelin-1 was reduced by losartan in NX and Sham rats. Vasorelaxation to acetylcholine was attenuated in untreated but not in losartan-treated NX rats, and experiments with Ca 2+ -activated K + channel blockers suggested that impaired endothelium-mediated response after NX was due to deficient relaxation via K + channels. Endothelium-independent relaxation to levcromakalim, adenosine triphosphate-sensitive K + channel agonist, was impaired in untreated but not in losartan-treated NX rats. Conclusion: Losartan reduced conduit artery vasoconstriction to endothelin-1 and augmented vasorelaxation via K + channels in NX rats, although blood pressure and renal function were unchanged. Therefore, AT 1 blockade confers functional benefits to large arteries in renal failure. |
| doi_str_mv | 10.1159/000076754 |
| format | Article |
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The effect of AT 1 blockade on conduit artery function in renal failure is unknown. Methods: The influence of 8-week losartan therapy (20 mg/kg/day) on tone of isolated main branch mesenteric arterial rings was studied in 5/6 nephrectomized (NX) rats. Blood and urine chemistry were examined, and AT 1 receptors quantified using autoradiography. Results: NX rats showed decreased creatinine clearance without change in blood pressure. Losartan did not influence these variables, although [ 125 I]-Sar1,Ile8-angiotensin II binding to renal AT 1 receptors was significantly prevented. Vasoconstriction to endothelin-1 was reduced by losartan in NX and Sham rats. Vasorelaxation to acetylcholine was attenuated in untreated but not in losartan-treated NX rats, and experiments with Ca 2+ -activated K + channel blockers suggested that impaired endothelium-mediated response after NX was due to deficient relaxation via K + channels. Endothelium-independent relaxation to levcromakalim, adenosine triphosphate-sensitive K + channel agonist, was impaired in untreated but not in losartan-treated NX rats. Conclusion: Losartan reduced conduit artery vasoconstriction to endothelin-1 and augmented vasorelaxation via K + channels in NX rats, although blood pressure and renal function were unchanged. Therefore, AT 1 blockade confers functional benefits to large arteries in renal failure.</description><identifier>ISSN: 0028-2766</identifier><identifier>ISSN: 1660-2137</identifier><identifier>ISSN: 1660-8151</identifier><identifier>EISSN: 1660-2137</identifier><identifier>EISSN: 2235-3186</identifier><identifier>DOI: 10.1159/000076754</identifier><identifier>PMID: 15056982</identifier><identifier>CODEN: NPRNAY</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Angiotensin II Type 1 Receptor Blockers ; Animals ; Biological and medical sciences ; Culture Techniques ; Endothelium, Vascular - physiopathology ; Kidney - chemistry ; Kidney Failure, Chronic - etiology ; Kidney Failure, Chronic - physiopathology ; Losartan - pharmacology ; Male ; Medical sciences ; Mesenteric Arteries - drug effects ; Mesenteric Arteries - physiopathology ; Nephrectomy ; Nephrology. Urinary tract diseases ; Original Paper ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 - analysis ; Vasoconstriction - drug effects ; Vasodilation - drug effects</subject><ispartof>Nephron, 2004-03, Vol.96 (3), p.p91-p98</ispartof><rights>2004 S. Karger AG, Basel</rights><rights>2004 INIST-CNRS</rights><rights>Copyright 2004 S. Karger AG, Basel</rights><rights>Copyright (c) 2004 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c304t-ca83a5b763a5842cf152d3b98c38d6492f010fc7720575007f981304d55bf8533</citedby><cites>FETCH-LOGICAL-c304t-ca83a5b763a5842cf152d3b98c38d6492f010fc7720575007f981304d55bf8533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15624026$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15056982$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kööbi, Peeter</creatorcontrib><creatorcontrib>Jolma, Pasi</creatorcontrib><creatorcontrib>Kalliovalkama, Jarkko</creatorcontrib><creatorcontrib>Tikkanen, Ilkka</creatorcontrib><creatorcontrib>Fan, Meng</creatorcontrib><creatorcontrib>Kähönen, Mika</creatorcontrib><creatorcontrib>Moilanen, Eeva</creatorcontrib><creatorcontrib>Pörsti, Ilkka</creatorcontrib><title>Effect of Angiotensin II Type 1 Receptor Blockade on Conduit Artery Tone in Subtotally Nephrectomized Rats</title><title>Nephron</title><addtitle>Nephron Physiol</addtitle><description>Background: Angiotensin II type 1 (AT 1 ) receptor antagonists provide end-organ protection and enhance resistance artery relaxation in uremia. The effect of AT 1 blockade on conduit artery function in renal failure is unknown. Methods: The influence of 8-week losartan therapy (20 mg/kg/day) on tone of isolated main branch mesenteric arterial rings was studied in 5/6 nephrectomized (NX) rats. Blood and urine chemistry were examined, and AT 1 receptors quantified using autoradiography. Results: NX rats showed decreased creatinine clearance without change in blood pressure. Losartan did not influence these variables, although [ 125 I]-Sar1,Ile8-angiotensin II binding to renal AT 1 receptors was significantly prevented. Vasoconstriction to endothelin-1 was reduced by losartan in NX and Sham rats. Vasorelaxation to acetylcholine was attenuated in untreated but not in losartan-treated NX rats, and experiments with Ca 2+ -activated K + channel blockers suggested that impaired endothelium-mediated response after NX was due to deficient relaxation via K + channels. Endothelium-independent relaxation to levcromakalim, adenosine triphosphate-sensitive K + channel agonist, was impaired in untreated but not in losartan-treated NX rats. Conclusion: Losartan reduced conduit artery vasoconstriction to endothelin-1 and augmented vasorelaxation via K + channels in NX rats, although blood pressure and renal function were unchanged. Therefore, AT 1 blockade confers functional benefits to large arteries in renal failure.</description><subject>Angiotensin II Type 1 Receptor Blockers</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Culture Techniques</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Kidney - chemistry</subject><subject>Kidney Failure, Chronic - etiology</subject><subject>Kidney Failure, Chronic - physiopathology</subject><subject>Losartan - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesenteric Arteries - drug effects</subject><subject>Mesenteric Arteries - physiopathology</subject><subject>Nephrectomy</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Original Paper</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Angiotensin, Type 1 - analysis</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasodilation - drug effects</subject><issn>0028-2766</issn><issn>1660-2137</issn><issn>1660-8151</issn><issn>1660-2137</issn><issn>2235-3186</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqF0c9rFDEUB_AgFrutHjwLEoQKPYwmmcmv47pUu1AU6noeMpmXOtvZZEwyh_WvN2WXWryYQ0Lg877h5SH0mpIPlHL9kZQlheTNM7SgQpCK0Vo-RwtCmKqYFOIUnaW0LVfWNPQFOqWccKEVW6DtlXNgMw4OL_3dEDL4NHi8XuPNfgJM8S1YmHKI-NMY7L3pAQePV8H385DxMmaIe7wJHnCp-j53OWQzjnv8FaafsQSH3fAbenxrcnqJTpwZE7w6nufox-erzeq6uvn2Zb1a3lS2Jk2urFG14Z0UZVcNs45y1tedVrZWvWg0c4QSZ6VkhEteGnda0VLZc945xev6HL0_5E4x_Joh5XY3JAvjaDyEObWSSqWVpv-FjJb_4_oh8d0_cBvm6EsTLZNNzaimvKDLA7IxpBTBtVMcdibuW0rahzG1j2Mq9u0xcO520P-Vx7kUcHEEJlkzumi8HdITJ1hDmCjuzcHdm3gH8REcnvkDBQifvQ</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Kööbi, Peeter</creator><creator>Jolma, Pasi</creator><creator>Kalliovalkama, Jarkko</creator><creator>Tikkanen, Ilkka</creator><creator>Fan, Meng</creator><creator>Kähönen, Mika</creator><creator>Moilanen, Eeva</creator><creator>Pörsti, Ilkka</creator><general>Karger</general><general>S. 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Urinary tract diseases</topic><topic>Original Paper</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Angiotensin, Type 1 - analysis</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kööbi, Peeter</creatorcontrib><creatorcontrib>Jolma, Pasi</creatorcontrib><creatorcontrib>Kalliovalkama, Jarkko</creatorcontrib><creatorcontrib>Tikkanen, Ilkka</creatorcontrib><creatorcontrib>Fan, Meng</creatorcontrib><creatorcontrib>Kähönen, Mika</creatorcontrib><creatorcontrib>Moilanen, Eeva</creatorcontrib><creatorcontrib>Pörsti, Ilkka</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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 China</collection><collection>SIRS Editorial</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Nephron</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kööbi, Peeter</au><au>Jolma, Pasi</au><au>Kalliovalkama, Jarkko</au><au>Tikkanen, Ilkka</au><au>Fan, Meng</au><au>Kähönen, Mika</au><au>Moilanen, Eeva</au><au>Pörsti, Ilkka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Angiotensin II Type 1 Receptor Blockade on Conduit Artery Tone in Subtotally Nephrectomized Rats</atitle><jtitle>Nephron</jtitle><addtitle>Nephron Physiol</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>96</volume><issue>3</issue><spage>p91</spage><epage>p98</epage><pages>p91-p98</pages><issn>0028-2766</issn><issn>1660-2137</issn><issn>1660-8151</issn><eissn>1660-2137</eissn><eissn>2235-3186</eissn><coden>NPRNAY</coden><abstract>Background: Angiotensin II type 1 (AT 1 ) receptor antagonists provide end-organ protection and enhance resistance artery relaxation in uremia. The effect of AT 1 blockade on conduit artery function in renal failure is unknown. Methods: The influence of 8-week losartan therapy (20 mg/kg/day) on tone of isolated main branch mesenteric arterial rings was studied in 5/6 nephrectomized (NX) rats. Blood and urine chemistry were examined, and AT 1 receptors quantified using autoradiography. Results: NX rats showed decreased creatinine clearance without change in blood pressure. Losartan did not influence these variables, although [ 125 I]-Sar1,Ile8-angiotensin II binding to renal AT 1 receptors was significantly prevented. Vasoconstriction to endothelin-1 was reduced by losartan in NX and Sham rats. Vasorelaxation to acetylcholine was attenuated in untreated but not in losartan-treated NX rats, and experiments with Ca 2+ -activated K + channel blockers suggested that impaired endothelium-mediated response after NX was due to deficient relaxation via K + channels. Endothelium-independent relaxation to levcromakalim, adenosine triphosphate-sensitive K + channel agonist, was impaired in untreated but not in losartan-treated NX rats. Conclusion: Losartan reduced conduit artery vasoconstriction to endothelin-1 and augmented vasorelaxation via K + channels in NX rats, although blood pressure and renal function were unchanged. Therefore, AT 1 blockade confers functional benefits to large arteries in renal failure.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>15056982</pmid><doi>10.1159/000076754</doi><tpages>1</tpages></addata></record> |
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| subjects | Angiotensin II Type 1 Receptor Blockers Animals Biological and medical sciences Culture Techniques Endothelium, Vascular - physiopathology Kidney - chemistry Kidney Failure, Chronic - etiology Kidney Failure, Chronic - physiopathology Losartan - pharmacology Male Medical sciences Mesenteric Arteries - drug effects Mesenteric Arteries - physiopathology Nephrectomy Nephrology. Urinary tract diseases Original Paper Rats Rats, Sprague-Dawley Receptor, Angiotensin, Type 1 - analysis Vasoconstriction - drug effects Vasodilation - drug effects |
| title | Effect of Angiotensin II Type 1 Receptor Blockade on Conduit Artery Tone in Subtotally Nephrectomized Rats |
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