Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats
: Background: Chronic portal hypertension is accompanied by a nitric oxide (NO) dependent vasodilation. Three isoforms of NO producing synthases (NOS) are characterized: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Sources of increased NO levels in chronic hypertension is di...
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| Veröffentlicht in: | Liver (Copenhagen) 2002-12, Vol.22 (6), p.441-450 |
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| creator | Stumm, Michael Martin D'Orazio, Daniel Sumanovski, Lazar Trajan Martin, Pierre-Yves Reichen, Juerg Sieber, Cornel Christian |
| description | : Background: Chronic portal hypertension is accompanied by a nitric oxide (NO) dependent vasodilation. Three isoforms of NO producing synthases (NOS) are characterized: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Sources of increased NO levels in chronic hypertension is disputed. Methods: To determine eNOS and iNOS expression in different organs of portal hypertensive and control rats, we divided Sprague‐Dawley rats in 6 groups: (1) Partial portal vein ligated rats, (2) Bile duct ligated rats, (3) Carbon tetrachloride treated rats, (4) Sham operated rats, (5) Untreated control rats, and (6) LPS treated rats. Immunohistochemistry (IHC) and immunoblotting (IB) using antibodies against eNOS or iNOS were carried out on samples from thymus, aorta, heart, lung, oesophagus, liver, spleen, kidney, pancreas, small and large intestine. Results: IHC revealed an even eNOS expression in all groups. Expression of iNOS was restricted to macrophages in organs of LPS treated and the thymus of rats. IB mirrored these results. Conclusion: In chronic portal hypertension, the main source for NO production depends on eNOS activity. |
| doi_str_mv | 10.1034/j.1600-0676.2002.01653.x |
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Three isoforms of NO producing synthases (NOS) are characterized: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Sources of increased NO levels in chronic hypertension is disputed. Methods: To determine eNOS and iNOS expression in different organs of portal hypertensive and control rats, we divided Sprague‐Dawley rats in 6 groups: (1) Partial portal vein ligated rats, (2) Bile duct ligated rats, (3) Carbon tetrachloride treated rats, (4) Sham operated rats, (5) Untreated control rats, and (6) LPS treated rats. Immunohistochemistry (IHC) and immunoblotting (IB) using antibodies against eNOS or iNOS were carried out on samples from thymus, aorta, heart, lung, oesophagus, liver, spleen, kidney, pancreas, small and large intestine. Results: IHC revealed an even eNOS expression in all groups. Expression of iNOS was restricted to macrophages in organs of LPS treated and the thymus of rats. IB mirrored these results. Conclusion: In chronic portal hypertension, the main source for NO production depends on eNOS activity.</description><identifier>ISSN: 0106-9543</identifier><identifier>EISSN: 1600-0676</identifier><identifier>DOI: 10.1034/j.1600-0676.2002.01653.x</identifier><identifier>PMID: 12445168</identifier><language>eng</language><publisher>Oxford, UK: Munksgaard International Publishers</publisher><subject>Animals ; Blotting, Western ; cirrhosis ; Disease Models, Animal ; Fluorescent Antibody Technique, Indirect ; Hypertension, Portal - enzymology ; Hypertension, Portal - etiology ; immunoblotting ; Immunoenzyme Techniques ; immunohistochemistry ; Liver Cirrhosis, Experimental - complications ; Liver Cirrhosis, Experimental - enzymology ; Macrophages - enzymology ; Male ; nitric oxide ; Nitric Oxide Synthase - biosynthesis ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; portal hypertension ; Rats ; Rats, Sprague-Dawley ; Thymus Gland - enzymology</subject><ispartof>Liver (Copenhagen), 2002-12, Vol.22 (6), p.441-450</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4323-6a483fdbb5328363730037bcf53ee995cffc75ccbe0d4aaa6e56fbeb76af43bb3</citedby><cites>FETCH-LOGICAL-c4323-6a483fdbb5328363730037bcf53ee995cffc75ccbe0d4aaa6e56fbeb76af43bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1034%2Fj.1600-0676.2002.01653.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1034%2Fj.1600-0676.2002.01653.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12445168$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stumm, Michael Martin</creatorcontrib><creatorcontrib>D'Orazio, Daniel</creatorcontrib><creatorcontrib>Sumanovski, Lazar Trajan</creatorcontrib><creatorcontrib>Martin, Pierre-Yves</creatorcontrib><creatorcontrib>Reichen, Juerg</creatorcontrib><creatorcontrib>Sieber, Cornel Christian</creatorcontrib><title>Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats</title><title>Liver (Copenhagen)</title><addtitle>Liver</addtitle><description>: Background: Chronic portal hypertension is accompanied by a nitric oxide (NO) dependent vasodilation. Three isoforms of NO producing synthases (NOS) are characterized: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Sources of increased NO levels in chronic hypertension is disputed. Methods: To determine eNOS and iNOS expression in different organs of portal hypertensive and control rats, we divided Sprague‐Dawley rats in 6 groups: (1) Partial portal vein ligated rats, (2) Bile duct ligated rats, (3) Carbon tetrachloride treated rats, (4) Sham operated rats, (5) Untreated control rats, and (6) LPS treated rats. Immunohistochemistry (IHC) and immunoblotting (IB) using antibodies against eNOS or iNOS were carried out on samples from thymus, aorta, heart, lung, oesophagus, liver, spleen, kidney, pancreas, small and large intestine. Results: IHC revealed an even eNOS expression in all groups. Expression of iNOS was restricted to macrophages in organs of LPS treated and the thymus of rats. IB mirrored these results. Conclusion: In chronic portal hypertension, the main source for NO production depends on eNOS activity.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>cirrhosis</subject><subject>Disease Models, Animal</subject><subject>Fluorescent Antibody Technique, Indirect</subject><subject>Hypertension, Portal - enzymology</subject><subject>Hypertension, Portal - etiology</subject><subject>immunoblotting</subject><subject>Immunoenzyme Techniques</subject><subject>immunohistochemistry</subject><subject>Liver Cirrhosis, Experimental - complications</subject><subject>Liver Cirrhosis, Experimental - enzymology</subject><subject>Macrophages - enzymology</subject><subject>Male</subject><subject>nitric oxide</subject><subject>Nitric Oxide Synthase - biosynthesis</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nitric Oxide Synthase Type III</subject><subject>portal hypertension</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Thymus Gland - enzymology</subject><issn>0106-9543</issn><issn>1600-0676</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1v0zAYgC0EYmXwF5BPnJZgx1_pgQMa25hUAZpgSFws23mjuqROZzvQ_nscWo0rJ7-yn-e19CCEKakpYfztpqaSkIpIJeuGkKYmVApW75-gxePDU7QglMhqKTg7Qy9S2pBCcSWeozPacC6obBcoXIVuzGsYvBkusJ0yDmPG5QL70E3O2wEucPA5eofHve8Ap0PIa5MKkHAHGVw2BSp4MePWDNiEDu_GmMu4PuwgZgjJ_wIcTU4v0bPeDAlenc5z9O366uvlx2r1-eb28v2qcpw1rJKGt6zvrBWsaZlkihHClHW9YADLpXB975RwzgLpuDFGgpC9Bauk6Tmzlp2jN8e9uzg-TJCy3vrkYBhMgHFKWjWq4Uy0BWyPoItjShF6vYt-a-JBU6Ln1nqj56R6Tqrn1vpva70v6uvTH5PdQvdPPMUtwLsj8NsPcPjvxXp1ez9Pxa-Ovk8Z9o--iT-1VEwJ_f3Tjf5xfS_uvtAP-o79AfeAnvU</recordid><startdate>200212</startdate><enddate>200212</enddate><creator>Stumm, Michael Martin</creator><creator>D'Orazio, Daniel</creator><creator>Sumanovski, Lazar Trajan</creator><creator>Martin, Pierre-Yves</creator><creator>Reichen, Juerg</creator><creator>Sieber, Cornel Christian</creator><general>Munksgaard International Publishers</general><scope>BSCLL</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></search><sort><creationdate>200212</creationdate><title>Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats</title><author>Stumm, Michael Martin ; D'Orazio, Daniel ; Sumanovski, Lazar Trajan ; Martin, Pierre-Yves ; Reichen, Juerg ; Sieber, Cornel Christian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4323-6a483fdbb5328363730037bcf53ee995cffc75ccbe0d4aaa6e56fbeb76af43bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Blotting, Western</topic><topic>cirrhosis</topic><topic>Disease Models, Animal</topic><topic>Fluorescent Antibody Technique, Indirect</topic><topic>Hypertension, Portal - enzymology</topic><topic>Hypertension, Portal - etiology</topic><topic>immunoblotting</topic><topic>Immunoenzyme Techniques</topic><topic>immunohistochemistry</topic><topic>Liver Cirrhosis, Experimental - complications</topic><topic>Liver Cirrhosis, Experimental - enzymology</topic><topic>Macrophages - enzymology</topic><topic>Male</topic><topic>nitric oxide</topic><topic>Nitric Oxide Synthase - biosynthesis</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Nitric Oxide Synthase Type III</topic><topic>portal hypertension</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Thymus Gland - enzymology</topic><toplevel>online_resources</toplevel><creatorcontrib>Stumm, Michael Martin</creatorcontrib><creatorcontrib>D'Orazio, Daniel</creatorcontrib><creatorcontrib>Sumanovski, Lazar Trajan</creatorcontrib><creatorcontrib>Martin, Pierre-Yves</creatorcontrib><creatorcontrib>Reichen, Juerg</creatorcontrib><creatorcontrib>Sieber, Cornel Christian</creatorcontrib><collection>Istex</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><jtitle>Liver (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stumm, Michael Martin</au><au>D'Orazio, Daniel</au><au>Sumanovski, Lazar Trajan</au><au>Martin, Pierre-Yves</au><au>Reichen, Juerg</au><au>Sieber, Cornel Christian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats</atitle><jtitle>Liver (Copenhagen)</jtitle><addtitle>Liver</addtitle><date>2002-12</date><risdate>2002</risdate><volume>22</volume><issue>6</issue><spage>441</spage><epage>450</epage><pages>441-450</pages><issn>0106-9543</issn><eissn>1600-0676</eissn><abstract>: Background: Chronic portal hypertension is accompanied by a nitric oxide (NO) dependent vasodilation. Three isoforms of NO producing synthases (NOS) are characterized: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Sources of increased NO levels in chronic hypertension is disputed. Methods: To determine eNOS and iNOS expression in different organs of portal hypertensive and control rats, we divided Sprague‐Dawley rats in 6 groups: (1) Partial portal vein ligated rats, (2) Bile duct ligated rats, (3) Carbon tetrachloride treated rats, (4) Sham operated rats, (5) Untreated control rats, and (6) LPS treated rats. Immunohistochemistry (IHC) and immunoblotting (IB) using antibodies against eNOS or iNOS were carried out on samples from thymus, aorta, heart, lung, oesophagus, liver, spleen, kidney, pancreas, small and large intestine. Results: IHC revealed an even eNOS expression in all groups. Expression of iNOS was restricted to macrophages in organs of LPS treated and the thymus of rats. IB mirrored these results. Conclusion: In chronic portal hypertension, the main source for NO production depends on eNOS activity.</abstract><cop>Oxford, UK</cop><pub>Munksgaard International Publishers</pub><pmid>12445168</pmid><doi>10.1034/j.1600-0676.2002.01653.x</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Blotting, Western cirrhosis Disease Models, Animal Fluorescent Antibody Technique, Indirect Hypertension, Portal - enzymology Hypertension, Portal - etiology immunoblotting Immunoenzyme Techniques immunohistochemistry Liver Cirrhosis, Experimental - complications Liver Cirrhosis, Experimental - enzymology Macrophages - enzymology Male nitric oxide Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III portal hypertension Rats Rats, Sprague-Dawley Thymus Gland - enzymology |
| title | Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats |
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