Enhanced nitric oxide synthase activity in portal hypertensive rabbits
Portal hypertension (PHT) is characterized by splanchnic hyperemia caused by a reduction in mesenteric vascular resistance. Mediators of this hyperemia include nitric oxide (NO). This is based on several reports indicating a marked splanchnic hyporesponsiveness in PHT to vasoconstrictor stimuli, bot...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 1995-08, Vol.22 (2), p.598-606 |
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| container_title | Hepatology (Baltimore, Md.) |
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| creator | Cahill, Paul A. Foster, Cory Redmond, Eileen M. Gingalewski, Cindy Wu, Yuping Sitzmann, James V. |
| description | Portal hypertension (PHT) is characterized by splanchnic hyperemia caused by a reduction in mesenteric vascular resistance. Mediators of this hyperemia include nitric oxide (NO). This is based on several reports indicating a marked splanchnic hyporesponsiveness in PHT to vasoconstrictor stimuli, both in vitro and in vivo, and a subsequent reversal using specific inhibitors of NO synthase (NOS). The objective of this study was to determine directly if the generation of NO is altered in PHT vasculature. Thus, we compared NOS activity in the hyperemic vasculature of normal rabbits and rabbits with PHT (after undergoing partial portal vein ligation). Nicotinamide adenine dinucleotide phosphate diaphorase staining indicated the presence of NOS within the vascular endothelium. Ca2+‐dependent NOS activity was significantly increased (P < .05) in PHT particulate fractions from the superior mesenteric artery and thoracic aorta, but not from the portal vein. There was no change in NOS activity within the cytosolic fractions. Arterial wall cyclic guanosine monophosphate (cGMP) levels and plasma nitrite levels were both significantly increased in PHT. These results show enhanced NOS activity in PHT hyperemic vessels concurrent with increased tissue cGMP levels. We conclude that enhanced NO synthesis contributes to the hyperdynamic circulation of PHT. (Hepatology 1995; 22:598–606.) |
| doi_str_mv | 10.1002/hep.1840220233 |
| format | Article |
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Mediators of this hyperemia include nitric oxide (NO). This is based on several reports indicating a marked splanchnic hyporesponsiveness in PHT to vasoconstrictor stimuli, both in vitro and in vivo, and a subsequent reversal using specific inhibitors of NO synthase (NOS). The objective of this study was to determine directly if the generation of NO is altered in PHT vasculature. Thus, we compared NOS activity in the hyperemic vasculature of normal rabbits and rabbits with PHT (after undergoing partial portal vein ligation). Nicotinamide adenine dinucleotide phosphate diaphorase staining indicated the presence of NOS within the vascular endothelium. Ca2+‐dependent NOS activity was significantly increased (P < .05) in PHT particulate fractions from the superior mesenteric artery and thoracic aorta, but not from the portal vein. There was no change in NOS activity within the cytosolic fractions. Arterial wall cyclic guanosine monophosphate (cGMP) levels and plasma nitrite levels were both significantly increased in PHT. These results show enhanced NOS activity in PHT hyperemic vessels concurrent with increased tissue cGMP levels. We conclude that enhanced NO synthesis contributes to the hyperdynamic circulation of PHT. (Hepatology 1995; 22:598–606.)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.1840220233</identifier><identifier>PMID: 7543437</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Philadelphia, PA: W.B. Saunders</publisher><subject>Amino Acid Oxidoreductases - antagonists & inhibitors ; Amino Acid Oxidoreductases - metabolism ; Animals ; Aorta, Thoracic - enzymology ; Arginine - analogs & derivatives ; Arginine - pharmacology ; Biological and medical sciences ; Calcium - pharmacology ; Cyclic GMP - metabolism ; Endothelium, Vascular - enzymology ; Gastroenterology. Liver. Pancreas. Abdomen ; Hemodynamics ; Hypertension, Portal - enzymology ; Hypertension, Portal - physiopathology ; Ligation ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Mesenteric Artery, Superior - enzymology ; NADPH Dehydrogenase - analysis ; NG-Nitroarginine Methyl Ester ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase ; Nitrites - blood ; Other diseases. Semiology ; Portal Vein - enzymology ; Portal Vein - surgery ; Rabbits</subject><ispartof>Hepatology (Baltimore, Md.), 1995-08, Vol.22 (2), p.598-606</ispartof><rights>Copyright © 1995 American Association for the Study of Liver Diseases</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3113-67ef44dc77b7a0ec5bb25c124e22a30fd2cfdf5561d89da615844f263e879a5d3</citedby><cites>FETCH-LOGICAL-c3113-67ef44dc77b7a0ec5bb25c124e22a30fd2cfdf5561d89da615844f263e879a5d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.1840220233$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.1840220233$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3640795$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7543437$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cahill, Paul A.</creatorcontrib><creatorcontrib>Foster, Cory</creatorcontrib><creatorcontrib>Redmond, Eileen M.</creatorcontrib><creatorcontrib>Gingalewski, Cindy</creatorcontrib><creatorcontrib>Wu, Yuping</creatorcontrib><creatorcontrib>Sitzmann, James V.</creatorcontrib><title>Enhanced nitric oxide synthase activity in portal hypertensive rabbits</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>Portal hypertension (PHT) is characterized by splanchnic hyperemia caused by a reduction in mesenteric vascular resistance. Mediators of this hyperemia include nitric oxide (NO). This is based on several reports indicating a marked splanchnic hyporesponsiveness in PHT to vasoconstrictor stimuli, both in vitro and in vivo, and a subsequent reversal using specific inhibitors of NO synthase (NOS). The objective of this study was to determine directly if the generation of NO is altered in PHT vasculature. Thus, we compared NOS activity in the hyperemic vasculature of normal rabbits and rabbits with PHT (after undergoing partial portal vein ligation). Nicotinamide adenine dinucleotide phosphate diaphorase staining indicated the presence of NOS within the vascular endothelium. Ca2+‐dependent NOS activity was significantly increased (P < .05) in PHT particulate fractions from the superior mesenteric artery and thoracic aorta, but not from the portal vein. There was no change in NOS activity within the cytosolic fractions. Arterial wall cyclic guanosine monophosphate (cGMP) levels and plasma nitrite levels were both significantly increased in PHT. These results show enhanced NOS activity in PHT hyperemic vessels concurrent with increased tissue cGMP levels. We conclude that enhanced NO synthesis contributes to the hyperdynamic circulation of PHT. (Hepatology 1995; 22:598–606.)</description><subject>Amino Acid Oxidoreductases - antagonists & inhibitors</subject><subject>Amino Acid Oxidoreductases - metabolism</subject><subject>Animals</subject><subject>Aorta, Thoracic - enzymology</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Calcium - pharmacology</subject><subject>Cyclic GMP - metabolism</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hemodynamics</subject><subject>Hypertension, Portal - enzymology</subject><subject>Hypertension, Portal - physiopathology</subject><subject>Ligation</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesenteric Artery, Superior - enzymology</subject><subject>NADPH Dehydrogenase - analysis</subject><subject>NG-Nitroarginine Methyl Ester</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase</subject><subject>Nitrites - blood</subject><subject>Other diseases. Semiology</subject><subject>Portal Vein - enzymology</subject><subject>Portal Vein - surgery</subject><subject>Rabbits</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1PwzAQhi0EKqWwsiFlQGwp_oyTEVUtRaoEA8yRY18UozQJtlvIvyeoUWFjuuF97r3Tg9A1wXOCMb2voJuTlGNKMWXsBE2JoDJmTOBTNMVU4jgjLDtHF96_Y4wzTtMJmkjBGWdyilbLplKNBhM1Njiro_bLGoh834RKeYiUDnZvQx_ZJupaF1QdVX0HLkDj7R4ip4rCBn-JzkpVe7ga5wy9rZavi3W8eX58WjxsYs0IYXEioeTcaCkLqTBoURRUaEI5UKoYLg3VpSmFSIhJM6MSIlLOS5owSGWmhGEzdHfo7Vz7sQMf8q31GupaNdDufC4l5wlPkwGcH0DtWu8dlHnn7Fa5Pic4_xGXD-LyX3HDws3YvCu2YI74aGrIb8dcea3q0g3WrD9iLOFYZmLAsgP2aWvo_zmar5cvf174BuR9huc</recordid><startdate>199508</startdate><enddate>199508</enddate><creator>Cahill, Paul A.</creator><creator>Foster, Cory</creator><creator>Redmond, Eileen M.</creator><creator>Gingalewski, Cindy</creator><creator>Wu, Yuping</creator><creator>Sitzmann, James V.</creator><general>W.B. Saunders</general><general>Wiley</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></search><sort><creationdate>199508</creationdate><title>Enhanced nitric oxide synthase activity in portal hypertensive rabbits</title><author>Cahill, Paul A. ; Foster, Cory ; Redmond, Eileen M. ; Gingalewski, Cindy ; Wu, Yuping ; Sitzmann, James V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3113-67ef44dc77b7a0ec5bb25c124e22a30fd2cfdf5561d89da615844f263e879a5d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Amino Acid Oxidoreductases - antagonists & inhibitors</topic><topic>Amino Acid Oxidoreductases - metabolism</topic><topic>Animals</topic><topic>Aorta, Thoracic - enzymology</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Calcium - pharmacology</topic><topic>Cyclic GMP - metabolism</topic><topic>Endothelium, Vascular - enzymology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hemodynamics</topic><topic>Hypertension, Portal - enzymology</topic><topic>Hypertension, Portal - physiopathology</topic><topic>Ligation</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesenteric Artery, Superior - enzymology</topic><topic>NADPH Dehydrogenase - analysis</topic><topic>NG-Nitroarginine Methyl Ester</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase</topic><topic>Nitrites - blood</topic><topic>Other diseases. Semiology</topic><topic>Portal Vein - enzymology</topic><topic>Portal Vein - surgery</topic><topic>Rabbits</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cahill, Paul A.</creatorcontrib><creatorcontrib>Foster, Cory</creatorcontrib><creatorcontrib>Redmond, Eileen M.</creatorcontrib><creatorcontrib>Gingalewski, Cindy</creatorcontrib><creatorcontrib>Wu, Yuping</creatorcontrib><creatorcontrib>Sitzmann, James V.</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><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cahill, Paul A.</au><au>Foster, Cory</au><au>Redmond, Eileen M.</au><au>Gingalewski, Cindy</au><au>Wu, Yuping</au><au>Sitzmann, James V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced nitric oxide synthase activity in portal hypertensive rabbits</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>1995-08</date><risdate>1995</risdate><volume>22</volume><issue>2</issue><spage>598</spage><epage>606</epage><pages>598-606</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>Portal hypertension (PHT) is characterized by splanchnic hyperemia caused by a reduction in mesenteric vascular resistance. Mediators of this hyperemia include nitric oxide (NO). This is based on several reports indicating a marked splanchnic hyporesponsiveness in PHT to vasoconstrictor stimuli, both in vitro and in vivo, and a subsequent reversal using specific inhibitors of NO synthase (NOS). The objective of this study was to determine directly if the generation of NO is altered in PHT vasculature. Thus, we compared NOS activity in the hyperemic vasculature of normal rabbits and rabbits with PHT (after undergoing partial portal vein ligation). Nicotinamide adenine dinucleotide phosphate diaphorase staining indicated the presence of NOS within the vascular endothelium. Ca2+‐dependent NOS activity was significantly increased (P < .05) in PHT particulate fractions from the superior mesenteric artery and thoracic aorta, but not from the portal vein. There was no change in NOS activity within the cytosolic fractions. Arterial wall cyclic guanosine monophosphate (cGMP) levels and plasma nitrite levels were both significantly increased in PHT. These results show enhanced NOS activity in PHT hyperemic vessels concurrent with increased tissue cGMP levels. We conclude that enhanced NO synthesis contributes to the hyperdynamic circulation of PHT. (Hepatology 1995; 22:598–606.)</abstract><cop>Philadelphia, PA</cop><pub>W.B. Saunders</pub><pmid>7543437</pmid><doi>10.1002/hep.1840220233</doi><tpages>9</tpages></addata></record> |
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| ispartof | Hepatology (Baltimore, Md.), 1995-08, Vol.22 (2), p.598-606 |
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| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Amino Acid Oxidoreductases - antagonists & inhibitors Amino Acid Oxidoreductases - metabolism Animals Aorta, Thoracic - enzymology Arginine - analogs & derivatives Arginine - pharmacology Biological and medical sciences Calcium - pharmacology Cyclic GMP - metabolism Endothelium, Vascular - enzymology Gastroenterology. Liver. Pancreas. Abdomen Hemodynamics Hypertension, Portal - enzymology Hypertension, Portal - physiopathology Ligation Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Mesenteric Artery, Superior - enzymology NADPH Dehydrogenase - analysis NG-Nitroarginine Methyl Ester Nitric Oxide - biosynthesis Nitric Oxide Synthase Nitrites - blood Other diseases. Semiology Portal Vein - enzymology Portal Vein - surgery Rabbits |
| title | Enhanced nitric oxide synthase activity in portal hypertensive rabbits |
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