Pulmonary Vasoconstriction and Hypertension in Mice With Targeted Disruption of the Endothelial Nitric Oxide Synthase (NOS 3) Gene
NO, synthesized in endothelial cells by endothelial NO synthase (NOS 3), is believed to be an important endogenous pulmonary vasodilator substance that contributes to the normal low pulmonary vascular resistance. To selectively investigate the role of NOS 3 in the pulmonary circulation, mice with ta...
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| Veröffentlicht in: | Circulation research 1997-07, Vol.81 (1), p.34-41 |
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| creator | Steudel, Wolfgang Ichinose, Fumito Huang, Paul L Hurford, William E Jones, Rosemary C Bevan, John A Fishman, Mark C Zapol, Warren M |
| description | NO, synthesized in endothelial cells by endothelial NO synthase (NOS 3), is believed to be an important endogenous pulmonary vasodilator substance that contributes to the normal low pulmonary vascular resistance. To selectively investigate the role of NOS 3 in the pulmonary circulation, mice with targeted disruption of the NOS 3 gene were studied. Pulmonary hemodynamics were studied by measuring pulmonary artery pressure, left ventricular end-diastolic pressure, and lower thoracic aortic flow by using a novel open-chest technique. Transient partial occlusion of the inferior vena cava was used to assess the pulmonary artery pressure-flow relationship. Tension developed by isolated pulmonary artery segments after acetylcholine stimulation was measured in vitro. The histological appearance of NOS 3-deficient and wild-type murine lungs was compared. NOS 3-deficient mice (n=27), when compared with wild-type mice (n=32), had pulmonary hypertension (pulmonary artery pressure, 19.0 +/- 0.8 versus 16.4 +/- 0.6 mm Hg [mean +/- SE]; P |
| doi_str_mv | 10.1161/01.RES.81.1.34 |
| format | Article |
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To selectively investigate the role of NOS 3 in the pulmonary circulation, mice with targeted disruption of the NOS 3 gene were studied. Pulmonary hemodynamics were studied by measuring pulmonary artery pressure, left ventricular end-diastolic pressure, and lower thoracic aortic flow by using a novel open-chest technique. Transient partial occlusion of the inferior vena cava was used to assess the pulmonary artery pressure-flow relationship. Tension developed by isolated pulmonary artery segments after acetylcholine stimulation was measured in vitro. The histological appearance of NOS 3-deficient and wild-type murine lungs was compared. NOS 3-deficient mice (n=27), when compared with wild-type mice (n=32), had pulmonary hypertension (pulmonary artery pressure, 19.0 +/- 0.8 versus 16.4 +/- 0.6 mm Hg [mean +/- SE]; P<.05) that was due to an increased total pulmonary resistance (62 +/- 6 versus 33 +/- 2 mm Hg [centered dot] min [centered dot] g [centered dot] mL sup -1; P<.001). In vitro, acetylcholine induced vasodilation in the main pulmonary arteries of wild-type but not NOS 3-deficient mice. The morphology of the lungs of NOS 3-deficient mice did not differ from that of wild-type mice. We conclude that NOS 3 is a key enzyme responsible for providing basal pulmonary NO release. Congenital NOS 3 deficiency produces mild pulmonary hypertension in mice. (Circ Res. 1997;81:34-41.)</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.81.1.34</identifier><identifier>PMID: 9201025</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Acetylcholine - pharmacology ; Animals ; Biological and medical sciences ; Data Interpretation, Statistical ; Endothelium - enzymology ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Targeting ; Hemodynamics ; Hemodynamics. Rheology ; Hypertension, Pulmonary - etiology ; Hypertension, Pulmonary - physiopathology ; In Vitro Techniques ; Lung - blood supply ; Lung - physiology ; Male ; Mice ; Nitric Oxide - biosynthesis ; Nitric Oxide - physiology ; Nitric Oxide Synthase - deficiency ; Nitric Oxide Synthase - genetics ; Pulmonary Artery - drug effects ; Pulmonary Artery - physiology ; Pulmonary Circulation ; Vascular Resistance ; Vasoconstriction ; Vasodilation ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 1997-07, Vol.81 (1), p.34-41</ispartof><rights>1997 American Heart Association, Inc.</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3995-1c3d3ce1a45e23ecace768f800660d1425850946c1f2d9fa829b8ce0700e22063</citedby><cites>FETCH-LOGICAL-c3995-1c3d3ce1a45e23ecace768f800660d1425850946c1f2d9fa829b8ce0700e22063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2739962$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9201025$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Steudel, Wolfgang</creatorcontrib><creatorcontrib>Ichinose, Fumito</creatorcontrib><creatorcontrib>Huang, Paul L</creatorcontrib><creatorcontrib>Hurford, William E</creatorcontrib><creatorcontrib>Jones, Rosemary C</creatorcontrib><creatorcontrib>Bevan, John A</creatorcontrib><creatorcontrib>Fishman, Mark C</creatorcontrib><creatorcontrib>Zapol, Warren M</creatorcontrib><title>Pulmonary Vasoconstriction and Hypertension in Mice With Targeted Disruption of the Endothelial Nitric Oxide Synthase (NOS 3) Gene</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>NO, synthesized in endothelial cells by endothelial NO synthase (NOS 3), is believed to be an important endogenous pulmonary vasodilator substance that contributes to the normal low pulmonary vascular resistance. To selectively investigate the role of NOS 3 in the pulmonary circulation, mice with targeted disruption of the NOS 3 gene were studied. Pulmonary hemodynamics were studied by measuring pulmonary artery pressure, left ventricular end-diastolic pressure, and lower thoracic aortic flow by using a novel open-chest technique. Transient partial occlusion of the inferior vena cava was used to assess the pulmonary artery pressure-flow relationship. Tension developed by isolated pulmonary artery segments after acetylcholine stimulation was measured in vitro. The histological appearance of NOS 3-deficient and wild-type murine lungs was compared. NOS 3-deficient mice (n=27), when compared with wild-type mice (n=32), had pulmonary hypertension (pulmonary artery pressure, 19.0 +/- 0.8 versus 16.4 +/- 0.6 mm Hg [mean +/- SE]; P<.05) that was due to an increased total pulmonary resistance (62 +/- 6 versus 33 +/- 2 mm Hg [centered dot] min [centered dot] g [centered dot] mL sup -1; P<.001). In vitro, acetylcholine induced vasodilation in the main pulmonary arteries of wild-type but not NOS 3-deficient mice. The morphology of the lungs of NOS 3-deficient mice did not differ from that of wild-type mice. We conclude that NOS 3 is a key enzyme responsible for providing basal pulmonary NO release. Congenital NOS 3 deficiency produces mild pulmonary hypertension in mice. (Circ Res. 1997;81:34-41.)</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Data Interpretation, Statistical</subject><subject>Endothelium - enzymology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Targeting</subject><subject>Hemodynamics</subject><subject>Hemodynamics. Rheology</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Lung - blood supply</subject><subject>Lung - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - deficiency</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Pulmonary Artery - drug effects</subject><subject>Pulmonary Artery - physiology</subject><subject>Pulmonary Circulation</subject><subject>Vascular Resistance</subject><subject>Vasoconstriction</subject><subject>Vasodilation</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kU1v1DAQhi0EKtvClRuSDwiVQ8KMnS8fUVlapNJFbIGj5ToT1pC1FztR2Su_nIRd9TTSzDOvNY8Ze4GQI1b4FjD_slznDeaYy-IRW2Apiqwoa3zMFgCgslpKeMpOU_oJgIUU6oSdKAEIolywv5_Hfhu8iXv-zaRgg09DdHZwwXPjW36131EcyKe54Tz_5Czx727Y8FsTf9BALX_vUhx3_zdCx4cN8aVvw1R7Z3p-4-Y8vvrjWuLrvR82JhE_v1mtuXzDL8nTM_akM32i58d6xr5-WN5eXGXXq8uPF--uMyuVKjO0spWW0BQlCUnWWKqrpmsAqgpaLETZlKCKymInWtWZRqi7xhLUACQEVPKMvT7k7mL4PVIa9NYlS31vPIUx6VpNSmohJjA_gDaGlCJ1ehfddlKkEfQsXQPqSbpuUKOWxbTw8pg83m2pfcCPlqf5q-PcJGv6LhpvXXrARD0dWM3vFgfsPvQDxfSrH-8p6g2Zftjo6S9BAooMlarnqyCbW6X8B33RmTg</recordid><startdate>199707</startdate><enddate>199707</enddate><creator>Steudel, Wolfgang</creator><creator>Ichinose, Fumito</creator><creator>Huang, Paul L</creator><creator>Hurford, William E</creator><creator>Jones, Rosemary C</creator><creator>Bevan, John A</creator><creator>Fishman, Mark C</creator><creator>Zapol, Warren M</creator><general>American Heart Association, Inc</general><general>Lippincott</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>199707</creationdate><title>Pulmonary Vasoconstriction and Hypertension in Mice With Targeted Disruption of the Endothelial Nitric Oxide Synthase (NOS 3) Gene</title><author>Steudel, Wolfgang ; Ichinose, Fumito ; Huang, Paul L ; Hurford, William E ; Jones, Rosemary C ; Bevan, John A ; Fishman, Mark C ; Zapol, Warren M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3995-1c3d3ce1a45e23ecace768f800660d1425850946c1f2d9fa829b8ce0700e22063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Data Interpretation, Statistical</topic><topic>Endothelium - enzymology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Targeting</topic><topic>Hemodynamics</topic><topic>Hemodynamics. Rheology</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Lung - blood supply</topic><topic>Lung - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - deficiency</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Pulmonary Artery - drug effects</topic><topic>Pulmonary Artery - physiology</topic><topic>Pulmonary Circulation</topic><topic>Vascular Resistance</topic><topic>Vasoconstriction</topic><topic>Vasodilation</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Steudel, Wolfgang</creatorcontrib><creatorcontrib>Ichinose, Fumito</creatorcontrib><creatorcontrib>Huang, Paul L</creatorcontrib><creatorcontrib>Hurford, William E</creatorcontrib><creatorcontrib>Jones, Rosemary C</creatorcontrib><creatorcontrib>Bevan, John A</creatorcontrib><creatorcontrib>Fishman, Mark C</creatorcontrib><creatorcontrib>Zapol, Warren M</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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Steudel, Wolfgang</au><au>Ichinose, Fumito</au><au>Huang, Paul L</au><au>Hurford, William E</au><au>Jones, Rosemary C</au><au>Bevan, John A</au><au>Fishman, Mark C</au><au>Zapol, Warren M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pulmonary Vasoconstriction and Hypertension in Mice With Targeted Disruption of the Endothelial Nitric Oxide Synthase (NOS 3) Gene</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1997-07</date><risdate>1997</risdate><volume>81</volume><issue>1</issue><spage>34</spage><epage>41</epage><pages>34-41</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>NO, synthesized in endothelial cells by endothelial NO synthase (NOS 3), is believed to be an important endogenous pulmonary vasodilator substance that contributes to the normal low pulmonary vascular resistance. To selectively investigate the role of NOS 3 in the pulmonary circulation, mice with targeted disruption of the NOS 3 gene were studied. Pulmonary hemodynamics were studied by measuring pulmonary artery pressure, left ventricular end-diastolic pressure, and lower thoracic aortic flow by using a novel open-chest technique. Transient partial occlusion of the inferior vena cava was used to assess the pulmonary artery pressure-flow relationship. Tension developed by isolated pulmonary artery segments after acetylcholine stimulation was measured in vitro. The histological appearance of NOS 3-deficient and wild-type murine lungs was compared. NOS 3-deficient mice (n=27), when compared with wild-type mice (n=32), had pulmonary hypertension (pulmonary artery pressure, 19.0 +/- 0.8 versus 16.4 +/- 0.6 mm Hg [mean +/- SE]; P<.05) that was due to an increased total pulmonary resistance (62 +/- 6 versus 33 +/- 2 mm Hg [centered dot] min [centered dot] g [centered dot] mL sup -1; P<.001). In vitro, acetylcholine induced vasodilation in the main pulmonary arteries of wild-type but not NOS 3-deficient mice. The morphology of the lungs of NOS 3-deficient mice did not differ from that of wild-type mice. We conclude that NOS 3 is a key enzyme responsible for providing basal pulmonary NO release. Congenital NOS 3 deficiency produces mild pulmonary hypertension in mice. (Circ Res. 1997;81:34-41.)</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9201025</pmid><doi>10.1161/01.RES.81.1.34</doi><tpages>8</tpages></addata></record> |
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| ispartof | Circulation research, 1997-07, Vol.81 (1), p.34-41 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Acetylcholine - pharmacology Animals Biological and medical sciences Data Interpretation, Statistical Endothelium - enzymology Female Fundamental and applied biological sciences. Psychology Gene Targeting Hemodynamics Hemodynamics. Rheology Hypertension, Pulmonary - etiology Hypertension, Pulmonary - physiopathology In Vitro Techniques Lung - blood supply Lung - physiology Male Mice Nitric Oxide - biosynthesis Nitric Oxide - physiology Nitric Oxide Synthase - deficiency Nitric Oxide Synthase - genetics Pulmonary Artery - drug effects Pulmonary Artery - physiology Pulmonary Circulation Vascular Resistance Vasoconstriction Vasodilation Vertebrates: cardiovascular system |
| title | Pulmonary Vasoconstriction and Hypertension in Mice With Targeted Disruption of the Endothelial Nitric Oxide Synthase (NOS 3) Gene |
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