Functional response of the rat kidney to inhibition of nitric oxide synthesis: role of cytochrome P450‐derived arachidonate metabolites
1 We tested the hypothesis that nitric oxide (NO) exerts a tonic inhibitory influence on cytochrome P450 (CYP450)‐dependent metabolism of arachidonic acid (AA). 2 Nω‐nitro‐L‐Arginine methyl ester (L‐NAME), an inhibitor of nitric oxide synthase (NOS), increased mean blood pressure (MBP), from 91±6 to...
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| Veröffentlicht in: | British journal of pharmacology 1998-11, Vol.125 (5), p.1065-1073 |
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| description | 1
We tested the hypothesis that nitric oxide (NO) exerts a tonic inhibitory influence on cytochrome P450 (CYP450)‐dependent metabolism of arachidonic acid (AA).
2
Nω‐nitro‐L‐Arginine methyl ester (L‐NAME), an inhibitor of nitric oxide synthase (NOS), increased mean blood pressure (MBP), from 91±6 to 137±5 mmHg, renal vascular resistance (RVR), from 9.9±0.6 to 27.4±2.5 mmHg ml−1 min−1, and reduced renal blood flow (RBF), from 9.8±0.7 to 6.5±0.6 ml min−1) and GFR from 1.2±0.2 to 0.6±0.2 ml 100 g−1 min−1) accompanied by diuresis (UV, 1.7±0.3 to 4.3±0.8 μl 100 g−1 min−1), and natriuresis (UNaV, 0.36±0.04 to 1.25±0.032 μmol 100 g−1 min−1).
3
12, 12 dibromododec‐enoic acid (DBDD), an inhibitor of ω hydroxylase, blunted L‐NAME‐induced changes in MBP, RVR, UV and UNaV by 63±8, 70±5, 45±8 and 42±9%, respectively, and fully reversed the reduction in GFR by L‐NAME. Clotrimazole, an inhibitor of the epoxygenase pathway of CYP450‐dependent AA metabolism, was without effect.
4
BMS182874 (5‐dimethylamino)‐N‐(3,4‐dimethyl‐5‐isoxazolyl)‐1‐naphthalenesulfonamide), an endothelin (ET)A receptor antagonist, also blunted the increases in MBP and RVR and the diuresis/natriuresis elicited by L‐NAME without affecting GFR.
5
Indomethacin blunted L‐NAME‐induced increases in RVR, UV and UNaV. BMS180291 (1S‐(1α,2α,3α.4α)]‐2‐[[3‐[4‐[(pentylamino)carbonyl]‐2‐oxazolyl] ‐ 7 ‐ oxabicyclo[2.2.1]hept ‐ 2 ‐yl]methyl]benzenepropanoic acid), an endoperoxide receptor antagonist, attenuated the pressor and renal haemodynamic but not the renal tubular effects of L‐NAME.
6
In conclusion, the renal functional effects of the CYP450‐derived mediator(s) expressed after inhibition of NOS with L‐NAME were prevented by inhibiting either CYP450 ω hydroxylase or cyclo‐oxygenase or by antagonizing either ETA or endoperoxide receptors. 20‐hydroxyeicosatetraenoic acid (20‐HETE) fulfils the salient properties of this mediator.
British Journal of Pharmacology (1998) 125, 1065–1073; doi:10.1038/sj.bjp.0702171 |
| doi_str_mv | 10.1038/sj.bjp.0702171 |
| format | Article |
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We tested the hypothesis that nitric oxide (NO) exerts a tonic inhibitory influence on cytochrome P450 (CYP450)‐dependent metabolism of arachidonic acid (AA).
2
Nω‐nitro‐L‐Arginine methyl ester (L‐NAME), an inhibitor of nitric oxide synthase (NOS), increased mean blood pressure (MBP), from 91±6 to 137±5 mmHg, renal vascular resistance (RVR), from 9.9±0.6 to 27.4±2.5 mmHg ml−1 min−1, and reduced renal blood flow (RBF), from 9.8±0.7 to 6.5±0.6 ml min−1) and GFR from 1.2±0.2 to 0.6±0.2 ml 100 g−1 min−1) accompanied by diuresis (UV, 1.7±0.3 to 4.3±0.8 μl 100 g−1 min−1), and natriuresis (UNaV, 0.36±0.04 to 1.25±0.032 μmol 100 g−1 min−1).
3
12, 12 dibromododec‐enoic acid (DBDD), an inhibitor of ω hydroxylase, blunted L‐NAME‐induced changes in MBP, RVR, UV and UNaV by 63±8, 70±5, 45±8 and 42±9%, respectively, and fully reversed the reduction in GFR by L‐NAME. Clotrimazole, an inhibitor of the epoxygenase pathway of CYP450‐dependent AA metabolism, was without effect.
4
BMS182874 (5‐dimethylamino)‐N‐(3,4‐dimethyl‐5‐isoxazolyl)‐1‐naphthalenesulfonamide), an endothelin (ET)A receptor antagonist, also blunted the increases in MBP and RVR and the diuresis/natriuresis elicited by L‐NAME without affecting GFR.
5
Indomethacin blunted L‐NAME‐induced increases in RVR, UV and UNaV. BMS180291 (1S‐(1α,2α,3α.4α)]‐2‐[[3‐[4‐[(pentylamino)carbonyl]‐2‐oxazolyl] ‐ 7 ‐ oxabicyclo[2.2.1]hept ‐ 2 ‐yl]methyl]benzenepropanoic acid), an endoperoxide receptor antagonist, attenuated the pressor and renal haemodynamic but not the renal tubular effects of L‐NAME.
6
In conclusion, the renal functional effects of the CYP450‐derived mediator(s) expressed after inhibition of NOS with L‐NAME were prevented by inhibiting either CYP450 ω hydroxylase or cyclo‐oxygenase or by antagonizing either ETA or endoperoxide receptors. 20‐hydroxyeicosatetraenoic acid (20‐HETE) fulfils the salient properties of this mediator.
British Journal of Pharmacology (1998) 125, 1065–1073; doi:10.1038/sj.bjp.0702171</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0702171</identifier><identifier>PMID: 9846646</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>20‐HETE ; Animals ; Arachidonic Acids - metabolism ; Biological and medical sciences ; cyclo‐oxygenase ; CYP450 ; Cytochrome P-450 Enzyme Inhibitors ; Cytochrome P-450 Enzyme System - metabolism ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - metabolism ; Endothelin Receptor Antagonists ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; Hydroxyeicosatetraenoic Acids - metabolism ; Kidney - drug effects ; Kidney - metabolism ; L‐NAME ; Male ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric oxide ; Nitric Oxide - biosynthesis ; Rats ; Rats, Sprague-Dawley ; Receptor, Endothelin A ; Receptors, Endothelin - metabolism ; Receptors, Prostaglandin - antagonists & inhibitors ; Receptors, Prostaglandin - metabolism ; Receptors, Thromboxane A2, Prostaglandin H2 ; renal function ; Vertebrates: urinary system ; Viral Proteins - antagonists & inhibitors ; Viral Proteins - metabolism</subject><ispartof>British journal of pharmacology, 1998-11, Vol.125 (5), p.1065-1073</ispartof><rights>1998 British Pharmacological Society</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1998, Nature Publishing Group 1998 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4584-7aedca2c1c15749fdb01f247ea6d26d9cef12da45400f2507cf869393b37c1e93</citedby><cites>FETCH-LOGICAL-c4584-7aedca2c1c15749fdb01f247ea6d26d9cef12da45400f2507cf869393b37c1e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1565677/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1565677/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1626123$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9846646$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oyekan, Adebayo O.</creatorcontrib><creatorcontrib>McGiff, J. C.</creatorcontrib><title>Functional response of the rat kidney to inhibition of nitric oxide synthesis: role of cytochrome P450‐derived arachidonate metabolites</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1
We tested the hypothesis that nitric oxide (NO) exerts a tonic inhibitory influence on cytochrome P450 (CYP450)‐dependent metabolism of arachidonic acid (AA).
2
Nω‐nitro‐L‐Arginine methyl ester (L‐NAME), an inhibitor of nitric oxide synthase (NOS), increased mean blood pressure (MBP), from 91±6 to 137±5 mmHg, renal vascular resistance (RVR), from 9.9±0.6 to 27.4±2.5 mmHg ml−1 min−1, and reduced renal blood flow (RBF), from 9.8±0.7 to 6.5±0.6 ml min−1) and GFR from 1.2±0.2 to 0.6±0.2 ml 100 g−1 min−1) accompanied by diuresis (UV, 1.7±0.3 to 4.3±0.8 μl 100 g−1 min−1), and natriuresis (UNaV, 0.36±0.04 to 1.25±0.032 μmol 100 g−1 min−1).
3
12, 12 dibromododec‐enoic acid (DBDD), an inhibitor of ω hydroxylase, blunted L‐NAME‐induced changes in MBP, RVR, UV and UNaV by 63±8, 70±5, 45±8 and 42±9%, respectively, and fully reversed the reduction in GFR by L‐NAME. Clotrimazole, an inhibitor of the epoxygenase pathway of CYP450‐dependent AA metabolism, was without effect.
4
BMS182874 (5‐dimethylamino)‐N‐(3,4‐dimethyl‐5‐isoxazolyl)‐1‐naphthalenesulfonamide), an endothelin (ET)A receptor antagonist, also blunted the increases in MBP and RVR and the diuresis/natriuresis elicited by L‐NAME without affecting GFR.
5
Indomethacin blunted L‐NAME‐induced increases in RVR, UV and UNaV. BMS180291 (1S‐(1α,2α,3α.4α)]‐2‐[[3‐[4‐[(pentylamino)carbonyl]‐2‐oxazolyl] ‐ 7 ‐ oxabicyclo[2.2.1]hept ‐ 2 ‐yl]methyl]benzenepropanoic acid), an endoperoxide receptor antagonist, attenuated the pressor and renal haemodynamic but not the renal tubular effects of L‐NAME.
6
In conclusion, the renal functional effects of the CYP450‐derived mediator(s) expressed after inhibition of NOS with L‐NAME were prevented by inhibiting either CYP450 ω hydroxylase or cyclo‐oxygenase or by antagonizing either ETA or endoperoxide receptors. 20‐hydroxyeicosatetraenoic acid (20‐HETE) fulfils the salient properties of this mediator.
British Journal of Pharmacology (1998) 125, 1065–1073; doi:10.1038/sj.bjp.0702171</description><subject>20‐HETE</subject><subject>Animals</subject><subject>Arachidonic Acids - metabolism</subject><subject>Biological and medical sciences</subject><subject>cyclo‐oxygenase</subject><subject>CYP450</subject><subject>Cytochrome P-450 Enzyme Inhibitors</subject><subject>Cytochrome P-450 Enzyme System - metabolism</subject><subject>DNA-Binding Proteins - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Endothelin Receptor Antagonists</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hydroxyeicosatetraenoic Acids - metabolism</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>L‐NAME</subject><subject>Male</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Endothelin A</subject><subject>Receptors, Endothelin - metabolism</subject><subject>Receptors, Prostaglandin - antagonists & inhibitors</subject><subject>Receptors, Prostaglandin - metabolism</subject><subject>Receptors, Thromboxane A2, Prostaglandin H2</subject><subject>renal function</subject><subject>Vertebrates: urinary system</subject><subject>Viral Proteins - antagonists & inhibitors</subject><subject>Viral Proteins - metabolism</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkTFv1DAYhi0EKkdhZUPygNhy2IljJwxIpaK0UiU6wGw59hfiI7EP29c2Gysbv5Ffgq8XFZiYPDzP976WXoSeU7KmpGpex82622zXRJCSCvoArSgTvKirhj5EK0KIKChtmsfoSYwbQjIU9RE6ahvGOeMr9ONs53Sy3qkRB4hb7yJg3-M0AA4q4a_WOJhx8ti6wXZ2r-65sylYjf2tNYDj7LIfbXyDgx_v7vWcvB6CnwBfsZr8-v7TQLDXYLAKSg_W5MYEeIKkOj_aBPEpetSrMcKz5T1Gn8_efzo9Ly4_frg4PbksNKsbVggFRqtSU01rwdredIT2JROguCm5aTX0tDSK1YyQvqyJ0H3D26qtukpoCm11jN4ecre7bspZ4FJQo9wGO6kwS6-s_Jc4O8gv_lrSmtdciBzwagkI_tsOYpKTjRrGUTnwuygFoYRnNYvrg6iDjzFAf19CidyPJ-NG5vHkMl4-ePH31-71Za3MXy5cRa3GPiinbfyTyktOyypr1UG7sSPM_ymV767OOWOs-g0uOrhG</recordid><startdate>199811</startdate><enddate>199811</enddate><creator>Oyekan, Adebayo O.</creator><creator>McGiff, J. C.</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</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>199811</creationdate><title>Functional response of the rat kidney to inhibition of nitric oxide synthesis: role of cytochrome P450‐derived arachidonate metabolites</title><author>Oyekan, Adebayo O. ; McGiff, J. C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4584-7aedca2c1c15749fdb01f247ea6d26d9cef12da45400f2507cf869393b37c1e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>20‐HETE</topic><topic>Animals</topic><topic>Arachidonic Acids - metabolism</topic><topic>Biological and medical sciences</topic><topic>cyclo‐oxygenase</topic><topic>CYP450</topic><topic>Cytochrome P-450 Enzyme Inhibitors</topic><topic>Cytochrome P-450 Enzyme System - metabolism</topic><topic>DNA-Binding Proteins - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Endothelin Receptor Antagonists</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hydroxyeicosatetraenoic Acids - metabolism</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>L‐NAME</topic><topic>Male</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Endothelin A</topic><topic>Receptors, Endothelin - metabolism</topic><topic>Receptors, Prostaglandin - antagonists & inhibitors</topic><topic>Receptors, Prostaglandin - metabolism</topic><topic>Receptors, Thromboxane A2, Prostaglandin H2</topic><topic>renal function</topic><topic>Vertebrates: urinary system</topic><topic>Viral Proteins - antagonists & inhibitors</topic><topic>Viral Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oyekan, Adebayo O.</creatorcontrib><creatorcontrib>McGiff, J. C.</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>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oyekan, Adebayo O.</au><au>McGiff, J. C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functional response of the rat kidney to inhibition of nitric oxide synthesis: role of cytochrome P450‐derived arachidonate metabolites</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1998-11</date><risdate>1998</risdate><volume>125</volume><issue>5</issue><spage>1065</spage><epage>1073</epage><pages>1065-1073</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1
We tested the hypothesis that nitric oxide (NO) exerts a tonic inhibitory influence on cytochrome P450 (CYP450)‐dependent metabolism of arachidonic acid (AA).
2
Nω‐nitro‐L‐Arginine methyl ester (L‐NAME), an inhibitor of nitric oxide synthase (NOS), increased mean blood pressure (MBP), from 91±6 to 137±5 mmHg, renal vascular resistance (RVR), from 9.9±0.6 to 27.4±2.5 mmHg ml−1 min−1, and reduced renal blood flow (RBF), from 9.8±0.7 to 6.5±0.6 ml min−1) and GFR from 1.2±0.2 to 0.6±0.2 ml 100 g−1 min−1) accompanied by diuresis (UV, 1.7±0.3 to 4.3±0.8 μl 100 g−1 min−1), and natriuresis (UNaV, 0.36±0.04 to 1.25±0.032 μmol 100 g−1 min−1).
3
12, 12 dibromododec‐enoic acid (DBDD), an inhibitor of ω hydroxylase, blunted L‐NAME‐induced changes in MBP, RVR, UV and UNaV by 63±8, 70±5, 45±8 and 42±9%, respectively, and fully reversed the reduction in GFR by L‐NAME. Clotrimazole, an inhibitor of the epoxygenase pathway of CYP450‐dependent AA metabolism, was without effect.
4
BMS182874 (5‐dimethylamino)‐N‐(3,4‐dimethyl‐5‐isoxazolyl)‐1‐naphthalenesulfonamide), an endothelin (ET)A receptor antagonist, also blunted the increases in MBP and RVR and the diuresis/natriuresis elicited by L‐NAME without affecting GFR.
5
Indomethacin blunted L‐NAME‐induced increases in RVR, UV and UNaV. BMS180291 (1S‐(1α,2α,3α.4α)]‐2‐[[3‐[4‐[(pentylamino)carbonyl]‐2‐oxazolyl] ‐ 7 ‐ oxabicyclo[2.2.1]hept ‐ 2 ‐yl]methyl]benzenepropanoic acid), an endoperoxide receptor antagonist, attenuated the pressor and renal haemodynamic but not the renal tubular effects of L‐NAME.
6
In conclusion, the renal functional effects of the CYP450‐derived mediator(s) expressed after inhibition of NOS with L‐NAME were prevented by inhibiting either CYP450 ω hydroxylase or cyclo‐oxygenase or by antagonizing either ETA or endoperoxide receptors. 20‐hydroxyeicosatetraenoic acid (20‐HETE) fulfils the salient properties of this mediator.
British Journal of Pharmacology (1998) 125, 1065–1073; doi:10.1038/sj.bjp.0702171</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9846646</pmid><doi>10.1038/sj.bjp.0702171</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Wiley Free Content; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | 20‐HETE Animals Arachidonic Acids - metabolism Biological and medical sciences cyclo‐oxygenase CYP450 Cytochrome P-450 Enzyme Inhibitors Cytochrome P-450 Enzyme System - metabolism DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - metabolism Endothelin Receptor Antagonists Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology Hydroxyeicosatetraenoic Acids - metabolism Kidney - drug effects Kidney - metabolism L‐NAME Male NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide Nitric Oxide - biosynthesis Rats Rats, Sprague-Dawley Receptor, Endothelin A Receptors, Endothelin - metabolism Receptors, Prostaglandin - antagonists & inhibitors Receptors, Prostaglandin - metabolism Receptors, Thromboxane A2, Prostaglandin H2 renal function Vertebrates: urinary system Viral Proteins - antagonists & inhibitors Viral Proteins - metabolism |
| title | Functional response of the rat kidney to inhibition of nitric oxide synthesis: role of cytochrome P450‐derived arachidonate metabolites |
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