Role of nitric oxide synthase activity in experimental ischemic acute renal failure in rats
To determine the role of nitric oxide (NO) in acute renal failure (ARF), we have studied the time course change activities to activity of nitric oxide synthase (NOS) isoform activities, both calcium dependent and independent NOS, in experimental ischemic ARF. We have also analyzed change activities...
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creator | Komurai, Mild Ishii, Yasuko Matsuoka, Fumiaki Toyama, Katsuhide Ominato, Masayuki Sato, Takeo Maeba, Teruhiko Kimura, Kenjiro Owada, Shigeru |
description | To determine the role of nitric oxide (NO) in acute renal failure (ARF), we have studied the time course change activities to activity of nitric oxide synthase (NOS) isoform activities, both calcium dependent and independent NOS, in experimental ischemic ARF. We have also analyzed change activities to activity of the NOS activities in both renal cortex and medulla. Male SD rats (n = 5) were inducted to ARF by ischemia-reperfusion injury and divided into the following groups; Control group (sham operation), Day 0 group, (measurement performed on that day of operation), Day 1 group, (measurement performed one day after induction of ARF), Day 3 group and Day 7 group. Measurement of NOS activity was based on the following principles; NO is synthesized from arginine by nitric oxide synthase (NOS) and NO is converted to NO2(-)/NO3(-)(NOx) by oxidation. Detection of the final metabolite of NO, NOx was done using flow injection method (Griess reaction). The results were, (1) calcium dependent NOS activity in the cortex and medulla decreased, however it increased in the recovery period in the renal cortex (Cortex; Control, 0.941 +/- 0.765, D0, 0.382 +/- 0.271, D1, 0.118 +/- 0.353, D3, 2.030 +/- 0.235, D7, 3.588 +/- 2.706, Medulla; Control, 1.469 +/- 0.531, D0, 0.766 +/- 0.156, D1, 0.828 +/- 0.187, D3, 2.078 +/- 0.094, D7, 1.289 +/- 0.313 micromol NOx produced/mg protein/30 min). (2) On the other hand, iNOS activity increased in the early phase of ARF, both in the cortex and medulla, but returned to control values during the recovery phase in cortex and was maintained at higher levels in the medulla (Cortex; Control, 0.333 +/- 0.250, D0, 0.583 +/- 0.428, D1, 1.167 +/- 0.262, D3, 0.250 +/- 0.077, D7, 0.452 +/- 0.292, Medulla; Control, 0.139 +/- 0.169, D0, 0.279 +/- 0.070, D1, 1.140 +/- 0.226, D3, 0.452 +/- 0.048, D7, 0.625 +/- 0.048 micromol NOx produced/mg protein/30 min). These findings suggest that the role of NOS in ARF are different for the different NOS isoforms and have anatomic heterogeneity. |
doi_str_mv | 10.1023/A:1022418831200 |
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We have also analyzed change activities to activity of the NOS activities in both renal cortex and medulla. Male SD rats (n = 5) were inducted to ARF by ischemia-reperfusion injury and divided into the following groups; Control group (sham operation), Day 0 group, (measurement performed on that day of operation), Day 1 group, (measurement performed one day after induction of ARF), Day 3 group and Day 7 group. Measurement of NOS activity was based on the following principles; NO is synthesized from arginine by nitric oxide synthase (NOS) and NO is converted to NO2(-)/NO3(-)(NOx) by oxidation. Detection of the final metabolite of NO, NOx was done using flow injection method (Griess reaction). The results were, (1) calcium dependent NOS activity in the cortex and medulla decreased, however it increased in the recovery period in the renal cortex (Cortex; Control, 0.941 +/- 0.765, D0, 0.382 +/- 0.271, D1, 0.118 +/- 0.353, D3, 2.030 +/- 0.235, D7, 3.588 +/- 2.706, Medulla; Control, 1.469 +/- 0.531, D0, 0.766 +/- 0.156, D1, 0.828 +/- 0.187, D3, 2.078 +/- 0.094, D7, 1.289 +/- 0.313 micromol NOx produced/mg protein/30 min). (2) On the other hand, iNOS activity increased in the early phase of ARF, both in the cortex and medulla, but returned to control values during the recovery phase in cortex and was maintained at higher levels in the medulla (Cortex; Control, 0.333 +/- 0.250, D0, 0.583 +/- 0.428, D1, 1.167 +/- 0.262, D3, 0.250 +/- 0.077, D7, 0.452 +/- 0.292, Medulla; Control, 0.139 +/- 0.169, D0, 0.279 +/- 0.070, D1, 1.140 +/- 0.226, D3, 0.452 +/- 0.048, D7, 0.625 +/- 0.048 micromol NOx produced/mg protein/30 min). These findings suggest that the role of NOS in ARF are different for the different NOS isoforms and have anatomic heterogeneity.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1023/A:1022418831200</identifier><identifier>PMID: 12701821</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Acute Kidney Injury - enzymology ; Acute Kidney Injury - metabolism ; Animals ; Body Weight ; Calcium ; Calcium - metabolism ; Disease Models, Animal ; Heterogeneity ; Humans ; Kidney - metabolism ; Kidneys ; Male ; Metabolites ; Models, Biological ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - physiology ; Protein Isoforms ; Proteins ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; Rodents ; Time Factors</subject><ispartof>Molecular and cellular biochemistry, 2003-02, Vol.244 (1-2), p.129-133</ispartof><rights>Kluwer Academic Publishers 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12701821$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Komurai, Mild</creatorcontrib><creatorcontrib>Ishii, Yasuko</creatorcontrib><creatorcontrib>Matsuoka, Fumiaki</creatorcontrib><creatorcontrib>Toyama, Katsuhide</creatorcontrib><creatorcontrib>Ominato, Masayuki</creatorcontrib><creatorcontrib>Sato, Takeo</creatorcontrib><creatorcontrib>Maeba, Teruhiko</creatorcontrib><creatorcontrib>Kimura, Kenjiro</creatorcontrib><creatorcontrib>Owada, Shigeru</creatorcontrib><title>Role of nitric oxide synthase activity in experimental ischemic acute renal failure in rats</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>To determine the role of nitric oxide (NO) in acute renal failure (ARF), we have studied the time course change activities to activity of nitric oxide synthase (NOS) isoform activities, both calcium dependent and independent NOS, in experimental ischemic ARF. We have also analyzed change activities to activity of the NOS activities in both renal cortex and medulla. Male SD rats (n = 5) were inducted to ARF by ischemia-reperfusion injury and divided into the following groups; Control group (sham operation), Day 0 group, (measurement performed on that day of operation), Day 1 group, (measurement performed one day after induction of ARF), Day 3 group and Day 7 group. Measurement of NOS activity was based on the following principles; NO is synthesized from arginine by nitric oxide synthase (NOS) and NO is converted to NO2(-)/NO3(-)(NOx) by oxidation. Detection of the final metabolite of NO, NOx was done using flow injection method (Griess reaction). The results were, (1) calcium dependent NOS activity in the cortex and medulla decreased, however it increased in the recovery period in the renal cortex (Cortex; Control, 0.941 +/- 0.765, D0, 0.382 +/- 0.271, D1, 0.118 +/- 0.353, D3, 2.030 +/- 0.235, D7, 3.588 +/- 2.706, Medulla; Control, 1.469 +/- 0.531, D0, 0.766 +/- 0.156, D1, 0.828 +/- 0.187, D3, 2.078 +/- 0.094, D7, 1.289 +/- 0.313 micromol NOx produced/mg protein/30 min). (2) On the other hand, iNOS activity increased in the early phase of ARF, both in the cortex and medulla, but returned to control values during the recovery phase in cortex and was maintained at higher levels in the medulla (Cortex; Control, 0.333 +/- 0.250, D0, 0.583 +/- 0.428, D1, 1.167 +/- 0.262, D3, 0.250 +/- 0.077, D7, 0.452 +/- 0.292, Medulla; Control, 0.139 +/- 0.169, D0, 0.279 +/- 0.070, D1, 1.140 +/- 0.226, D3, 0.452 +/- 0.048, D7, 0.625 +/- 0.048 micromol NOx produced/mg protein/30 min). These findings suggest that the role of NOS in ARF are different for the different NOS isoforms and have anatomic heterogeneity.</description><subject>Acute Kidney Injury - enzymology</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Animals</subject><subject>Body Weight</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Disease Models, Animal</subject><subject>Heterogeneity</subject><subject>Humans</subject><subject>Kidney - metabolism</subject><subject>Kidneys</subject><subject>Male</subject><subject>Metabolites</subject><subject>Models, Biological</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - physiology</subject><subject>Protein Isoforms</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury</subject><subject>Rodents</subject><subject>Time Factors</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpd0EtLBDEMAOAiiruunr1J8eBtNGnn6U0WX7AgiJ48DJ1Ohu0yL9uO7P57K64XIRAIX0ISxs4RrhGEvLm7DUnEmOcSBcABm2OSySgusDhkc5AAUY5ZNmMnzm0AMAQesxmKDDAXOGcfr0NLfGh4b7w1mg9bUxN3u96vlSOutDdfxu-46TltR7Kmo96rlhun19SFBqUnT9xSH4qNMu1k6Qdb5d0pO2pU6-hsnxfs_eH-bfkUrV4en5d3q2gUMvZRUmBeCUgh06lOqjwRRCoDEDEkKBopqhQqrRVWVSWU0CoJStVFLNIaCWq5YFe_c0c7fE7kfNmF9ahtVU_D5MpMYpGLVAR4-Q9uhsmGzYNJUswwT9KALvZoqjqqyzHcrOyu_PuZ_AbogW3o</recordid><startdate>200302</startdate><enddate>200302</enddate><creator>Komurai, Mild</creator><creator>Ishii, Yasuko</creator><creator>Matsuoka, Fumiaki</creator><creator>Toyama, Katsuhide</creator><creator>Ominato, Masayuki</creator><creator>Sato, Takeo</creator><creator>Maeba, Teruhiko</creator><creator>Kimura, Kenjiro</creator><creator>Owada, Shigeru</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>AEUYN</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><scope>7X8</scope></search><sort><creationdate>200302</creationdate><title>Role of nitric oxide synthase activity in experimental ischemic acute renal failure in rats</title><author>Komurai, Mild ; Ishii, Yasuko ; Matsuoka, Fumiaki ; Toyama, Katsuhide ; Ominato, Masayuki ; Sato, Takeo ; Maeba, Teruhiko ; Kimura, Kenjiro ; Owada, Shigeru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p234t-5918b20607c6c5b852eea700240512f32b60bcca1bbb2a2ca5c5bad9426d1e0d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acute Kidney Injury - enzymology</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Animals</topic><topic>Body Weight</topic><topic>Calcium</topic><topic>Calcium - metabolism</topic><topic>Disease Models, Animal</topic><topic>Heterogeneity</topic><topic>Humans</topic><topic>Kidney - metabolism</topic><topic>Kidneys</topic><topic>Male</topic><topic>Metabolites</topic><topic>Models, Biological</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - physiology</topic><topic>Protein Isoforms</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury</topic><topic>Rodents</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Komurai, Mild</creatorcontrib><creatorcontrib>Ishii, Yasuko</creatorcontrib><creatorcontrib>Matsuoka, Fumiaki</creatorcontrib><creatorcontrib>Toyama, Katsuhide</creatorcontrib><creatorcontrib>Ominato, Masayuki</creatorcontrib><creatorcontrib>Sato, Takeo</creatorcontrib><creatorcontrib>Maeba, Teruhiko</creatorcontrib><creatorcontrib>Kimura, Kenjiro</creatorcontrib><creatorcontrib>Owada, Shigeru</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 & 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>Health & 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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>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 & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</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><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Komurai, Mild</au><au>Ishii, Yasuko</au><au>Matsuoka, Fumiaki</au><au>Toyama, Katsuhide</au><au>Ominato, Masayuki</au><au>Sato, Takeo</au><au>Maeba, Teruhiko</au><au>Kimura, Kenjiro</au><au>Owada, Shigeru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of nitric oxide synthase activity in experimental ischemic acute renal failure in rats</atitle><jtitle>Molecular and cellular biochemistry</jtitle><addtitle>Mol Cell Biochem</addtitle><date>2003-02</date><risdate>2003</risdate><volume>244</volume><issue>1-2</issue><spage>129</spage><epage>133</epage><pages>129-133</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>To determine the role of nitric oxide (NO) in acute renal failure (ARF), we have studied the time course change activities to activity of nitric oxide synthase (NOS) isoform activities, both calcium dependent and independent NOS, in experimental ischemic ARF. We have also analyzed change activities to activity of the NOS activities in both renal cortex and medulla. Male SD rats (n = 5) were inducted to ARF by ischemia-reperfusion injury and divided into the following groups; Control group (sham operation), Day 0 group, (measurement performed on that day of operation), Day 1 group, (measurement performed one day after induction of ARF), Day 3 group and Day 7 group. Measurement of NOS activity was based on the following principles; NO is synthesized from arginine by nitric oxide synthase (NOS) and NO is converted to NO2(-)/NO3(-)(NOx) by oxidation. Detection of the final metabolite of NO, NOx was done using flow injection method (Griess reaction). The results were, (1) calcium dependent NOS activity in the cortex and medulla decreased, however it increased in the recovery period in the renal cortex (Cortex; Control, 0.941 +/- 0.765, D0, 0.382 +/- 0.271, D1, 0.118 +/- 0.353, D3, 2.030 +/- 0.235, D7, 3.588 +/- 2.706, Medulla; Control, 1.469 +/- 0.531, D0, 0.766 +/- 0.156, D1, 0.828 +/- 0.187, D3, 2.078 +/- 0.094, D7, 1.289 +/- 0.313 micromol NOx produced/mg protein/30 min). (2) On the other hand, iNOS activity increased in the early phase of ARF, both in the cortex and medulla, but returned to control values during the recovery phase in cortex and was maintained at higher levels in the medulla (Cortex; Control, 0.333 +/- 0.250, D0, 0.583 +/- 0.428, D1, 1.167 +/- 0.262, D3, 0.250 +/- 0.077, D7, 0.452 +/- 0.292, Medulla; Control, 0.139 +/- 0.169, D0, 0.279 +/- 0.070, D1, 1.140 +/- 0.226, D3, 0.452 +/- 0.048, D7, 0.625 +/- 0.048 micromol NOx produced/mg protein/30 min). These findings suggest that the role of NOS in ARF are different for the different NOS isoforms and have anatomic heterogeneity.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>12701821</pmid><doi>10.1023/A:1022418831200</doi><tpages>5</tpages></addata></record> |
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subjects | Acute Kidney Injury - enzymology Acute Kidney Injury - metabolism Animals Body Weight Calcium Calcium - metabolism Disease Models, Animal Heterogeneity Humans Kidney - metabolism Kidneys Male Metabolites Models, Biological Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase - physiology Protein Isoforms Proteins Rats Rats, Sprague-Dawley Reperfusion Injury Rodents Time Factors |
title | Role of nitric oxide synthase activity in experimental ischemic acute renal failure in rats |
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