Protection of wistar Furth rats from chronic renal disease is associated with maintained renal nitric oxide synthase
Wistar Furth (WF) rats do not develop renal injury after severe reduction of renal mass. Because clinical and animal studies suggested that nitric oxide (NO) deficiency occurs and may contribute to chronic renal disease (CRD), the status of the NO system in WF versus Sprague Dawley (SD) rats was exa...
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Veröffentlicht in: | Journal of the American Society of Nephrology 2003-10, Vol.14 (10), p.2526-2533 |
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description | Wistar Furth (WF) rats do not develop renal injury after severe reduction of renal mass. Because clinical and animal studies suggested that nitric oxide (NO) deficiency occurs and may contribute to chronic renal disease (CRD), the status of the NO system in WF versus Sprague Dawley (SD) rats was examined with the 5/6 renal ablation/infarction (A/I) model of CRD. Eleven weeks after A/I, SD rats developed proteinuria, severe kidney damage, decreased renal function, and marked decreases in total and renal NO synthase (NOS), specifically neuronal NOS. In contrast, WF rats exhibited elevated baseline and maintained post-A/I total NO production, with no decrease in renal cortex NOS activity despite a decrease in remnant neuronal NOS abundance. When low-dose chronic Nomega-nitro-L-arginine methyl ester treatment was added for WF A/I-treated rats, rapid progression of CRD was observed. In conclusion, elevated NO production in WF rats was associated with protection from the progression of CRD after renal mass reduction. The protection might be attributable to greater total and renal NO-generating capacity and increased nephron number, compared with SD rats. NOS inhibition rendered WF rats susceptible to progression, suggesting a possible critical threshold for NO production, below which renal injury occurs. |
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Because clinical and animal studies suggested that nitric oxide (NO) deficiency occurs and may contribute to chronic renal disease (CRD), the status of the NO system in WF versus Sprague Dawley (SD) rats was examined with the 5/6 renal ablation/infarction (A/I) model of CRD. Eleven weeks after A/I, SD rats developed proteinuria, severe kidney damage, decreased renal function, and marked decreases in total and renal NO synthase (NOS), specifically neuronal NOS. In contrast, WF rats exhibited elevated baseline and maintained post-A/I total NO production, with no decrease in renal cortex NOS activity despite a decrease in remnant neuronal NOS abundance. When low-dose chronic Nomega-nitro-L-arginine methyl ester treatment was added for WF A/I-treated rats, rapid progression of CRD was observed. In conclusion, elevated NO production in WF rats was associated with protection from the progression of CRD after renal mass reduction. The protection might be attributable to greater total and renal NO-generating capacity and increased nephron number, compared with SD rats. NOS inhibition rendered WF rats susceptible to progression, suggesting a possible critical threshold for NO production, below which renal injury occurs.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1097/01.ASN.0000086476.48686.7D</identifier><identifier>PMID: 14514730</identifier><identifier>CODEN: JASNEU</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Blood Urea Nitrogen ; Creatinine - blood ; Enzyme Inhibitors - pharmacology ; Kidney Cortex - enzymology ; Kidney Failure, Chronic - metabolism ; Kidney Medulla - enzymology ; Male ; Medical sciences ; Nephrectomy ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type III ; Rats ; Rats, Inbred WF ; Renal failure</subject><ispartof>Journal of the American Society of Nephrology, 2003-10, Vol.14 (10), p.2526-2533</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-a3a36979ec6ac23f824bd552a90be34c9123e7e800c27a15688834228ea00bb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15180103$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14514730$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ERDELY, Aaron</creatorcontrib><creatorcontrib>WAGNER, Laszlo</creatorcontrib><creatorcontrib>MULLER, Veronica</creatorcontrib><creatorcontrib>SZABO, Attila</creatorcontrib><creatorcontrib>BAYLIS, Chris</creatorcontrib><title>Protection of wistar Furth rats from chronic renal disease is associated with maintained renal nitric oxide synthase</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>Wistar Furth (WF) rats do not develop renal injury after severe reduction of renal mass. Because clinical and animal studies suggested that nitric oxide (NO) deficiency occurs and may contribute to chronic renal disease (CRD), the status of the NO system in WF versus Sprague Dawley (SD) rats was examined with the 5/6 renal ablation/infarction (A/I) model of CRD. Eleven weeks after A/I, SD rats developed proteinuria, severe kidney damage, decreased renal function, and marked decreases in total and renal NO synthase (NOS), specifically neuronal NOS. In contrast, WF rats exhibited elevated baseline and maintained post-A/I total NO production, with no decrease in renal cortex NOS activity despite a decrease in remnant neuronal NOS abundance. When low-dose chronic Nomega-nitro-L-arginine methyl ester treatment was added for WF A/I-treated rats, rapid progression of CRD was observed. In conclusion, elevated NO production in WF rats was associated with protection from the progression of CRD after renal mass reduction. The protection might be attributable to greater total and renal NO-generating capacity and increased nephron number, compared with SD rats. NOS inhibition rendered WF rats susceptible to progression, suggesting a possible critical threshold for NO production, below which renal injury occurs.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Urea Nitrogen</subject><subject>Creatinine - blood</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Kidney Cortex - enzymology</subject><subject>Kidney Failure, Chronic - metabolism</subject><subject>Kidney Medulla - enzymology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrectomy</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type I</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Rats</subject><subject>Rats, Inbred WF</subject><subject>Renal failure</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkV1rFDEUhoMo9kP_ggRB72bMdzJeCKW1KhQV7H04k8m4kZmkJtlq_71pd3E1EHJCnuck5EXoJSU9JYN-Q2h_9u1zT-6HUUKrXhhlVK8vHqFjKjnvuJDkcauJUJ1Smh-hk1J-EEIl0_opOqJCUqE5OUb1a07VuxpSxGnGv0KpkPHlNtcNzlALnnNasdvkFIPD2UdY8BSKh-JxKBhKSS5A9VNTm7JCiLXNtt-xMdTcxPQ7TB6Xu1g3zXyGnsywFP98v56i68v31-cfu6svHz6dn111TkhWO-DA1aAH7xQ4xmfDxDhJyWAgo-fCDZRxr70hxDENVCpjDBeMGQ-EjCM_Re92bW-24-on52PNsNibHFbIdzZBsP-fxLCx39OtZVro9qWtwet9g5x-bn2pdg3F-WWB6NO2WC01NZSxBr7dgS6nUrKf_15Cib3PzBJqW2b2kJl9yMzqiya_-PeZB3UfUgNe7QEoDpY5Q3ShHDhJDaGE8z_d4aMS</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>ERDELY, Aaron</creator><creator>WAGNER, Laszlo</creator><creator>MULLER, Veronica</creator><creator>SZABO, Attila</creator><creator>BAYLIS, Chris</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><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><scope>5PM</scope></search><sort><creationdate>20031001</creationdate><title>Protection of wistar Furth rats from chronic renal disease is associated with maintained renal nitric oxide synthase</title><author>ERDELY, Aaron ; WAGNER, Laszlo ; MULLER, Veronica ; SZABO, Attila ; BAYLIS, Chris</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-a3a36979ec6ac23f824bd552a90be34c9123e7e800c27a15688834228ea00bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Urea Nitrogen</topic><topic>Creatinine - blood</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Kidney Cortex - enzymology</topic><topic>Kidney Failure, Chronic - metabolism</topic><topic>Kidney Medulla - enzymology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrectomy</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type I</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Rats</topic><topic>Rats, Inbred WF</topic><topic>Renal failure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ERDELY, Aaron</creatorcontrib><creatorcontrib>WAGNER, Laszlo</creatorcontrib><creatorcontrib>MULLER, Veronica</creatorcontrib><creatorcontrib>SZABO, Attila</creatorcontrib><creatorcontrib>BAYLIS, Chris</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ERDELY, Aaron</au><au>WAGNER, Laszlo</au><au>MULLER, Veronica</au><au>SZABO, Attila</au><au>BAYLIS, Chris</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protection of wistar Furth rats from chronic renal disease is associated with maintained renal nitric oxide synthase</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>14</volume><issue>10</issue><spage>2526</spage><epage>2533</epage><pages>2526-2533</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><coden>JASNEU</coden><abstract>Wistar Furth (WF) rats do not develop renal injury after severe reduction of renal mass. Because clinical and animal studies suggested that nitric oxide (NO) deficiency occurs and may contribute to chronic renal disease (CRD), the status of the NO system in WF versus Sprague Dawley (SD) rats was examined with the 5/6 renal ablation/infarction (A/I) model of CRD. Eleven weeks after A/I, SD rats developed proteinuria, severe kidney damage, decreased renal function, and marked decreases in total and renal NO synthase (NOS), specifically neuronal NOS. In contrast, WF rats exhibited elevated baseline and maintained post-A/I total NO production, with no decrease in renal cortex NOS activity despite a decrease in remnant neuronal NOS abundance. When low-dose chronic Nomega-nitro-L-arginine methyl ester treatment was added for WF A/I-treated rats, rapid progression of CRD was observed. In conclusion, elevated NO production in WF rats was associated with protection from the progression of CRD after renal mass reduction. The protection might be attributable to greater total and renal NO-generating capacity and increased nephron number, compared with SD rats. NOS inhibition rendered WF rats susceptible to progression, suggesting a possible critical threshold for NO production, below which renal injury occurs.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>14514730</pmid><doi>10.1097/01.ASN.0000086476.48686.7D</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences Blood Urea Nitrogen Creatinine - blood Enzyme Inhibitors - pharmacology Kidney Cortex - enzymology Kidney Failure, Chronic - metabolism Kidney Medulla - enzymology Male Medical sciences Nephrectomy Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Nitric Oxide - metabolism Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type I Nitric Oxide Synthase Type III Rats Rats, Inbred WF Renal failure |
title | Protection of wistar Furth rats from chronic renal disease is associated with maintained renal nitric oxide synthase |
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