Nitric Oxide Buffers Renal Medullary Vasoconstriction Induced by Prostaglandins Synthesis Blockade
The aim of this study was to examine whether nitric oxide (NO) buffers the renal medullary vasoconstriction induced by a prostaglandins (PG) synthesis inhibitor. Daily blood pressure measurements were made with implanted catheters and changes in cortical blood flow (CBF) and medullary blood flow (MB...
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| Veröffentlicht in: | Hypertension Research 2001, Vol.24(6), pp.699-704 |
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| container_title | Hypertension Research |
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| creator | NAKANISHI, Kazushige CHINEN, Akira SAITO, Yoshihito HAMADA, Kaoru HARA, Noriko NAGAI, Yohko |
| description | The aim of this study was to examine whether nitric oxide (NO) buffers the renal medullary vasoconstriction induced by a prostaglandins (PG) synthesis inhibitor. Daily blood pressure measurements were made with implanted catheters and changes in cortical blood flow (CBF) and medullary blood flow (MBF) were determined by implanted optical fibers and laser-Doppler flow measurement techniques in conscious rats. Sodium and water balance were also determined. Infusion of meclofenamate, a nonisozyme-specific cyclooxygenase (COX) inhibitor, at 5μg/kg/min over 4 consecutive days (n=12 rats) elicited a transitory increase (p |
| doi_str_mv | 10.1291/hypres.24.699 |
| format | Article |
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Daily blood pressure measurements were made with implanted catheters and changes in cortical blood flow (CBF) and medullary blood flow (MBF) were determined by implanted optical fibers and laser-Doppler flow measurement techniques in conscious rats. Sodium and water balance were also determined. Infusion of meclofenamate, a nonisozyme-specific cyclooxygenase (COX) inhibitor, at 5μg/kg/min over 4 consecutive days (n=12 rats) elicited a transitory increase (p<0.05) in mean arterial pressure (MAP) and a transitory decrease (p<0.05) in MBF and sodium excretion without altering CBF. In contrast, the simultaneous infusion of meclofenamate and NG-nitro-L-arginine methyl ester (L-NAME, 0.8μg/kg/min), a NO synthesis inhibitor, over 4 consecutive days (n=12) produced a continuous increase (p<0.01) in MAP and a continuous decrease (p<0.05) in MBF and sodium excretion without altering CBF. The results of this study suggest that the renal medullary vasoconstrictor effects and sodium retention induced by meclofenamate are enhanced by a subpressor dose of L-NAME, and that NO may buffer the renal medullary vasoconstriction induced by the blockade of PG synthesis in conscious rats. (Hypertens Res 2001; 24: 699-704)</description><identifier>ISSN: 0916-9636</identifier><identifier>EISSN: 1348-4214</identifier><identifier>DOI: 10.1291/hypres.24.699</identifier><identifier>PMID: 11768730</identifier><language>eng</language><publisher>England: The Japanese Society of Hypertension</publisher><subject>Animals ; Blood Pressure - drug effects ; Buffers ; Cyclooxygenase Inhibitors - administration & dosage ; Cyclooxygenase Inhibitors - pharmacology ; Drug Synergism ; Enzyme Inhibitors - pharmacology ; hypertension ; Injections, Intravenous ; Kidney Medulla - blood supply ; Male ; Meclofenamic Acid - pharmacology ; Natriuresis - drug effects ; NG-Nitroarginine Methyl Ester - administration & dosage ; NG-Nitroarginine Methyl Ester - pharmacology ; nitric oxide ; Nitric Oxide - physiology ; prostaglandin ; Prostaglandin Antagonists - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Regional Blood Flow - drug effects ; renal medullary blood flow ; Time Factors ; Vasoconstriction - physiology</subject><ispartof>Hypertension Research, 2001, Vol.24(6), pp.699-704</ispartof><rights>2001 by the Japanese Society of Hypertension</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c578t-8570a7b1474fe347ced64dbdbf01f1b1ed2c34a319592b478504bc2aac89c553</citedby><cites>FETCH-LOGICAL-c578t-8570a7b1474fe347ced64dbdbf01f1b1ed2c34a319592b478504bc2aac89c553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11768730$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NAKANISHI, Kazushige</creatorcontrib><creatorcontrib>CHINEN, Akira</creatorcontrib><creatorcontrib>SAITO, Yoshihito</creatorcontrib><creatorcontrib>HAMADA, Kaoru</creatorcontrib><creatorcontrib>HARA, Noriko</creatorcontrib><creatorcontrib>NAGAI, Yohko</creatorcontrib><title>Nitric Oxide Buffers Renal Medullary Vasoconstriction Induced by Prostaglandins Synthesis Blockade</title><title>Hypertension Research</title><addtitle>Hypertension Research</addtitle><description>The aim of this study was to examine whether nitric oxide (NO) buffers the renal medullary vasoconstriction induced by a prostaglandins (PG) synthesis inhibitor. Daily blood pressure measurements were made with implanted catheters and changes in cortical blood flow (CBF) and medullary blood flow (MBF) were determined by implanted optical fibers and laser-Doppler flow measurement techniques in conscious rats. Sodium and water balance were also determined. Infusion of meclofenamate, a nonisozyme-specific cyclooxygenase (COX) inhibitor, at 5μg/kg/min over 4 consecutive days (n=12 rats) elicited a transitory increase (p<0.05) in mean arterial pressure (MAP) and a transitory decrease (p<0.05) in MBF and sodium excretion without altering CBF. In contrast, the simultaneous infusion of meclofenamate and NG-nitro-L-arginine methyl ester (L-NAME, 0.8μg/kg/min), a NO synthesis inhibitor, over 4 consecutive days (n=12) produced a continuous increase (p<0.01) in MAP and a continuous decrease (p<0.05) in MBF and sodium excretion without altering CBF. The results of this study suggest that the renal medullary vasoconstrictor effects and sodium retention induced by meclofenamate are enhanced by a subpressor dose of L-NAME, and that NO may buffer the renal medullary vasoconstriction induced by the blockade of PG synthesis in conscious rats. (Hypertens Res 2001; 24: 699-704)</description><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Buffers</subject><subject>Cyclooxygenase Inhibitors - administration & dosage</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Drug Synergism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>hypertension</subject><subject>Injections, Intravenous</subject><subject>Kidney Medulla - blood supply</subject><subject>Male</subject><subject>Meclofenamic Acid - pharmacology</subject><subject>Natriuresis - drug effects</subject><subject>NG-Nitroarginine Methyl Ester - administration & dosage</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>nitric oxide</subject><subject>Nitric Oxide - physiology</subject><subject>prostaglandin</subject><subject>Prostaglandin Antagonists - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reference Values</subject><subject>Regional Blood Flow - drug effects</subject><subject>renal medullary blood flow</subject><subject>Time Factors</subject><subject>Vasoconstriction - physiology</subject><issn>0916-9636</issn><issn>1348-4214</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkMtOwzAQRS0EoqWwZIv8Ayl-JY6XtOJRqVAEFdvIr1CX1KnsRCJ_T6qgwmZmMUdXdw4A1xhNMRH4dtPtg41TwqaZECdgjCnLE0YwOwVjJHCWiIxmI3AR4xYhkqcCn4MRxjzLOUVjoF5cE5yGq29nLJy1ZWlDhG_Wywo-W9NWlQwd_JCx1rWPB7RxtYcLb1ptDVQdfA11bORnJb1xPsL3zjcbG12Es6rWX9LYS3BWyiraq989AeuH-_X8KVmuHhfzu2WiU543SZ5yJLnCjLPSUsb7-IwZZVSJcIkVtoZoyiTFIhVEMZ6niClNpNS50GlKJyAZYnVfKAZbFvvgdn37AqPioKoYVBWEFb2qnr8Z-H2rdtb80b9uemA2ANvDf_YIyNA4Xdn_ccPoU49HvZGhsJ7-AFFWgKI</recordid><startdate>2001</startdate><enddate>2001</enddate><creator>NAKANISHI, Kazushige</creator><creator>CHINEN, Akira</creator><creator>SAITO, Yoshihito</creator><creator>HAMADA, Kaoru</creator><creator>HARA, Noriko</creator><creator>NAGAI, Yohko</creator><general>The Japanese Society of Hypertension</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>2001</creationdate><title>Nitric Oxide Buffers Renal Medullary Vasoconstriction Induced by Prostaglandins Synthesis Blockade</title><author>NAKANISHI, Kazushige ; CHINEN, Akira ; SAITO, Yoshihito ; HAMADA, Kaoru ; HARA, Noriko ; NAGAI, Yohko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c578t-8570a7b1474fe347ced64dbdbf01f1b1ed2c34a319592b478504bc2aac89c553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Buffers</topic><topic>Cyclooxygenase Inhibitors - administration & dosage</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Drug Synergism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>hypertension</topic><topic>Injections, Intravenous</topic><topic>Kidney Medulla - blood supply</topic><topic>Male</topic><topic>Meclofenamic Acid - pharmacology</topic><topic>Natriuresis - drug effects</topic><topic>NG-Nitroarginine Methyl Ester - administration & dosage</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>nitric oxide</topic><topic>Nitric Oxide - physiology</topic><topic>prostaglandin</topic><topic>Prostaglandin Antagonists - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reference Values</topic><topic>Regional Blood Flow - drug effects</topic><topic>renal medullary blood flow</topic><topic>Time Factors</topic><topic>Vasoconstriction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NAKANISHI, Kazushige</creatorcontrib><creatorcontrib>CHINEN, Akira</creatorcontrib><creatorcontrib>SAITO, Yoshihito</creatorcontrib><creatorcontrib>HAMADA, Kaoru</creatorcontrib><creatorcontrib>HARA, Noriko</creatorcontrib><creatorcontrib>NAGAI, Yohko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Hypertension Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAKANISHI, Kazushige</au><au>CHINEN, Akira</au><au>SAITO, Yoshihito</au><au>HAMADA, Kaoru</au><au>HARA, Noriko</au><au>NAGAI, Yohko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric Oxide Buffers Renal Medullary Vasoconstriction Induced by Prostaglandins Synthesis Blockade</atitle><jtitle>Hypertension Research</jtitle><addtitle>Hypertension Research</addtitle><date>2001</date><risdate>2001</risdate><volume>24</volume><issue>6</issue><spage>699</spage><epage>704</epage><pages>699-704</pages><issn>0916-9636</issn><eissn>1348-4214</eissn><abstract>The aim of this study was to examine whether nitric oxide (NO) buffers the renal medullary vasoconstriction induced by a prostaglandins (PG) synthesis inhibitor. Daily blood pressure measurements were made with implanted catheters and changes in cortical blood flow (CBF) and medullary blood flow (MBF) were determined by implanted optical fibers and laser-Doppler flow measurement techniques in conscious rats. Sodium and water balance were also determined. Infusion of meclofenamate, a nonisozyme-specific cyclooxygenase (COX) inhibitor, at 5μg/kg/min over 4 consecutive days (n=12 rats) elicited a transitory increase (p<0.05) in mean arterial pressure (MAP) and a transitory decrease (p<0.05) in MBF and sodium excretion without altering CBF. In contrast, the simultaneous infusion of meclofenamate and NG-nitro-L-arginine methyl ester (L-NAME, 0.8μg/kg/min), a NO synthesis inhibitor, over 4 consecutive days (n=12) produced a continuous increase (p<0.01) in MAP and a continuous decrease (p<0.05) in MBF and sodium excretion without altering CBF. The results of this study suggest that the renal medullary vasoconstrictor effects and sodium retention induced by meclofenamate are enhanced by a subpressor dose of L-NAME, and that NO may buffer the renal medullary vasoconstriction induced by the blockade of PG synthesis in conscious rats. (Hypertens Res 2001; 24: 699-704)</abstract><cop>England</cop><pub>The Japanese Society of Hypertension</pub><pmid>11768730</pmid><doi>10.1291/hypres.24.699</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Blood Pressure - drug effects Buffers Cyclooxygenase Inhibitors - administration & dosage Cyclooxygenase Inhibitors - pharmacology Drug Synergism Enzyme Inhibitors - pharmacology hypertension Injections, Intravenous Kidney Medulla - blood supply Male Meclofenamic Acid - pharmacology Natriuresis - drug effects NG-Nitroarginine Methyl Ester - administration & dosage NG-Nitroarginine Methyl Ester - pharmacology nitric oxide Nitric Oxide - physiology prostaglandin Prostaglandin Antagonists - pharmacology Rats Rats, Sprague-Dawley Reference Values Regional Blood Flow - drug effects renal medullary blood flow Time Factors Vasoconstriction - physiology |
| title | Nitric Oxide Buffers Renal Medullary Vasoconstriction Induced by Prostaglandins Synthesis Blockade |
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