A novel inhibitor of inducible nitric oxide synthase, ONO-1714, does not ameliorate hypoxia-induced pulmonary hypertension in rats
A recent study showed that long-term administration of the inducible nitric oxide synthase (iNOS) inhibitor L-NIL reduced the development of pulmonary hypertension. The purpose of the present study was to identify the effect of an another iNOS inhibitor, ONO-1714, on the development of pulmonary hyp...
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| Veröffentlicht in: | Lung 2007-09, Vol.185 (5), p.303-308 |
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| creator | Jiang, Bao Hua Maruyama, Junko Yokochi, Ayumu Mitani, Yoshihide Maruyama, Kazuo |
| description | A recent study showed that long-term administration of the inducible nitric oxide synthase (iNOS) inhibitor L-NIL reduced the development of pulmonary hypertension. The purpose of the present study was to identify the effect of an another iNOS inhibitor, ONO-1714, on the development of pulmonary hypertensive vascular changes in chronic hypoxic pulmonary hypertension in rats. ONO-1714 was administered to rats exposed to hypobaric hypoxia (air at 380 mmHg) for 10 days. Muscularization of normally nonmuscular peripheral arteries and medial hypertrophy of normally muscular arteries were assessed by light microscopy. iNOS mRNA and protein levels of the lung were assessed in normal and hypoxic rats. Chronic hypoxia induced pulmonary hypertension, right ventricular hypertrophy, and hypertensive pulmonary vascular changes. Although an acute single injection of ONO-1714 induced a significant increase in mean pulmonary artery pressure in chronic hypoxic pulmonary hypertensive rats, the increase was slight and transient. There were no significant differences among rats with and without long-term administration of ONO-1714 in pulmonary artery pressure, right ventricular hypertrophy, medial wall thickness of muscular arteries, and the percentage of muscularized arteries at the alveolar wall and duct levels. Although there was a significantly increased expression of iNOS as assessed with the reverse-transcription polymerase chain reaction in rats that were exposed to 10 days of hypobaric hypoxia, we could not detect a significant level of iNOS protein by Western blotting. ONO-1714 does not have a therapeutic role in preventing the development of chronic hypoxic pulmonary hypertension. |
| doi_str_mv | 10.1007/s00408-007-9024-z |
| format | Article |
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The purpose of the present study was to identify the effect of an another iNOS inhibitor, ONO-1714, on the development of pulmonary hypertensive vascular changes in chronic hypoxic pulmonary hypertension in rats. ONO-1714 was administered to rats exposed to hypobaric hypoxia (air at 380 mmHg) for 10 days. Muscularization of normally nonmuscular peripheral arteries and medial hypertrophy of normally muscular arteries were assessed by light microscopy. iNOS mRNA and protein levels of the lung were assessed in normal and hypoxic rats. Chronic hypoxia induced pulmonary hypertension, right ventricular hypertrophy, and hypertensive pulmonary vascular changes. Although an acute single injection of ONO-1714 induced a significant increase in mean pulmonary artery pressure in chronic hypoxic pulmonary hypertensive rats, the increase was slight and transient. There were no significant differences among rats with and without long-term administration of ONO-1714 in pulmonary artery pressure, right ventricular hypertrophy, medial wall thickness of muscular arteries, and the percentage of muscularized arteries at the alveolar wall and duct levels. Although there was a significantly increased expression of iNOS as assessed with the reverse-transcription polymerase chain reaction in rats that were exposed to 10 days of hypobaric hypoxia, we could not detect a significant level of iNOS protein by Western blotting. ONO-1714 does not have a therapeutic role in preventing the development of chronic hypoxic pulmonary hypertension.</description><identifier>ISSN: 0341-2040</identifier><identifier>EISSN: 1432-1750</identifier><identifier>DOI: 10.1007/s00408-007-9024-z</identifier><identifier>PMID: 17721804</identifier><identifier>CODEN: LUNGD9</identifier><language>eng</language><publisher>United States: Springer</publisher><subject>Alveoli ; Amidines - pharmacology ; Amidines - therapeutic use ; Animals ; Antihypertensive Agents - pharmacology ; Antihypertensive Agents - therapeutic use ; Arteries ; Blood Pressure - drug effects ; Blotting, Western ; Body Weight - drug effects ; Chemical inhibitors ; Complications and side effects ; Disease Models, Animal ; Dosage and administration ; Drug therapy ; Enzyme Inhibitors - pharmacology ; Enzyme Inhibitors - therapeutic use ; Heart ; Hematocrit ; Heterocyclic Compounds, 2-Ring - pharmacology ; Heterocyclic Compounds, 2-Ring - therapeutic use ; Hypertension ; Hypertension, Pulmonary - complications ; Hypertension, Pulmonary - enzymology ; Hypertension, Pulmonary - etiology ; Hypertension, Pulmonary - pathology ; Hypertension, Pulmonary - physiopathology ; Hypertension, Pulmonary - prevention & control ; Hypertrophy ; Hypertrophy, Right Ventricular - enzymology ; Hypertrophy, Right Ventricular - etiology ; Hypertrophy, Right Ventricular - prevention & control ; Hypoxia ; Hypoxia - complications ; Hypoxia - drug therapy ; Hypoxia - enzymology ; Hypoxia - pathology ; Hypoxia - physiopathology ; Inhibitor drugs ; Inhibitors ; Light microscopy ; Lung - blood supply ; Lung - drug effects ; Lung - enzymology ; Lung - pathology ; Male ; Nitric oxide ; Nitric Oxide Synthase Type II - antagonists & inhibitors ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Nitric-oxide synthase ; Optical microscopy ; Polymerase chain reaction ; Proteins ; Pulmonary arteries ; Pulmonary artery ; Pulmonary Artery - drug effects ; Pulmonary Artery - pathology ; Pulmonary Artery - physiopathology ; Pulmonary hypertension ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Rodents ; Time Factors ; Veins & arteries ; Ventricle ; Western blotting</subject><ispartof>Lung, 2007-09, Vol.185 (5), p.303-308</ispartof><rights>COPYRIGHT 2007 Springer</rights><rights>Springer Science+Business Media, LLC 2007</rights><rights>Springer Science+Business Media, LLC 2007.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-bbaf19caaa1ea3c8d14e576fed66719ac6c6ab11f464d21c3593ffa2bc705d023</citedby><cites>FETCH-LOGICAL-c385t-bbaf19caaa1ea3c8d14e576fed66719ac6c6ab11f464d21c3593ffa2bc705d023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17721804$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Bao Hua</creatorcontrib><creatorcontrib>Maruyama, Junko</creatorcontrib><creatorcontrib>Yokochi, Ayumu</creatorcontrib><creatorcontrib>Mitani, Yoshihide</creatorcontrib><creatorcontrib>Maruyama, Kazuo</creatorcontrib><title>A novel inhibitor of inducible nitric oxide synthase, ONO-1714, does not ameliorate hypoxia-induced pulmonary hypertension in rats</title><title>Lung</title><addtitle>Lung</addtitle><description>A recent study showed that long-term administration of the inducible nitric oxide synthase (iNOS) inhibitor L-NIL reduced the development of pulmonary hypertension. The purpose of the present study was to identify the effect of an another iNOS inhibitor, ONO-1714, on the development of pulmonary hypertensive vascular changes in chronic hypoxic pulmonary hypertension in rats. ONO-1714 was administered to rats exposed to hypobaric hypoxia (air at 380 mmHg) for 10 days. Muscularization of normally nonmuscular peripheral arteries and medial hypertrophy of normally muscular arteries were assessed by light microscopy. iNOS mRNA and protein levels of the lung were assessed in normal and hypoxic rats. Chronic hypoxia induced pulmonary hypertension, right ventricular hypertrophy, and hypertensive pulmonary vascular changes. Although an acute single injection of ONO-1714 induced a significant increase in mean pulmonary artery pressure in chronic hypoxic pulmonary hypertensive rats, the increase was slight and transient. There were no significant differences among rats with and without long-term administration of ONO-1714 in pulmonary artery pressure, right ventricular hypertrophy, medial wall thickness of muscular arteries, and the percentage of muscularized arteries at the alveolar wall and duct levels. Although there was a significantly increased expression of iNOS as assessed with the reverse-transcription polymerase chain reaction in rats that were exposed to 10 days of hypobaric hypoxia, we could not detect a significant level of iNOS protein by Western blotting. ONO-1714 does not have a therapeutic role in preventing the development of chronic hypoxic pulmonary hypertension.</description><subject>Alveoli</subject><subject>Amidines - pharmacology</subject><subject>Amidines - therapeutic use</subject><subject>Animals</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Arteries</subject><subject>Blood Pressure - drug effects</subject><subject>Blotting, Western</subject><subject>Body Weight - drug effects</subject><subject>Chemical inhibitors</subject><subject>Complications and side effects</subject><subject>Disease Models, Animal</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Heart</subject><subject>Hematocrit</subject><subject>Heterocyclic Compounds, 2-Ring - pharmacology</subject><subject>Heterocyclic Compounds, 2-Ring - therapeutic use</subject><subject>Hypertension</subject><subject>Hypertension, Pulmonary - complications</subject><subject>Hypertension, Pulmonary - enzymology</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - pathology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>Hypertension, Pulmonary - prevention & control</subject><subject>Hypertrophy</subject><subject>Hypertrophy, Right Ventricular - enzymology</subject><subject>Hypertrophy, Right Ventricular - etiology</subject><subject>Hypertrophy, Right Ventricular - prevention & control</subject><subject>Hypoxia</subject><subject>Hypoxia - complications</subject><subject>Hypoxia - drug therapy</subject><subject>Hypoxia - enzymology</subject><subject>Hypoxia - pathology</subject><subject>Hypoxia - physiopathology</subject><subject>Inhibitor drugs</subject><subject>Inhibitors</subject><subject>Light microscopy</subject><subject>Lung - blood supply</subject><subject>Lung - drug effects</subject><subject>Lung - enzymology</subject><subject>Lung - pathology</subject><subject>Male</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase Type II - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Optical microscopy</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Pulmonary arteries</subject><subject>Pulmonary artery</subject><subject>Pulmonary Artery - drug effects</subject><subject>Pulmonary Artery - pathology</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Pulmonary hypertension</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Time Factors</subject><subject>Veins & arteries</subject><subject>Ventricle</subject><subject>Western blotting</subject><issn>0341-2040</issn><issn>1432-1750</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kU-LFDEQxYMo7rj6AbxIUPC0ralOOt19HBb_weJc9BzS6Wo7SzoZk_Ti7NFPbsYZWBA8pUJ-r16lHiEvgb0Dxtr3iTHBuqqUVc9qUd0_IhsQvK6gbdhjsmFcQFUX5oI8S-mWMWglNE_JBbRtDR0TG_J7S324Q0etn-1gc4g0TOUyrsYODqm3OVpDwy87Ik0Hn2ed8Iruvu6KCYgrOgZMpUWmekFnQ9QZ6XzYF4Gu_rbBke5XtwSv4-H4gjGjTzb44kILnp6TJ5N2CV-cz0vy_eOHb9efq5vdpy_X25vK8K7J1TDoCXqjtQbU3HQjCGxaOeEoZQu9NtJIPQBMQoqxBsObnk-TrgfTsmZkNb8kb0999zH8XDFltdhk0DntMaxJya6WEhgU8M0_4G1Yoy-zqUKITkjWyEK9_i_FQXayb-DB84d2qGbULs8puDWX_ye1LStsgMmuLyCcQBNDShEntY92KStTwNQxbHUKWx3LY9jqvmhenSdYhwXHB8U5Xf4H5PqlNA</recordid><startdate>20070901</startdate><enddate>20070901</enddate><creator>Jiang, Bao Hua</creator><creator>Maruyama, Junko</creator><creator>Yokochi, Ayumu</creator><creator>Mitani, Yoshihide</creator><creator>Maruyama, Kazuo</creator><general>Springer</general><general>Springer Nature B.V</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><scope>3V.</scope><scope>7QL</scope><scope>7RV</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20070901</creationdate><title>A novel inhibitor of inducible nitric oxide synthase, ONO-1714, does not ameliorate hypoxia-induced pulmonary hypertension in rats</title><author>Jiang, Bao Hua ; Maruyama, Junko ; Yokochi, Ayumu ; Mitani, Yoshihide ; Maruyama, Kazuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-bbaf19caaa1ea3c8d14e576fed66719ac6c6ab11f464d21c3593ffa2bc705d023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Alveoli</topic><topic>Amidines - pharmacology</topic><topic>Amidines - therapeutic use</topic><topic>Animals</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Arteries</topic><topic>Blood Pressure - drug effects</topic><topic>Blotting, Western</topic><topic>Body Weight - drug effects</topic><topic>Chemical inhibitors</topic><topic>Complications and side effects</topic><topic>Disease Models, Animal</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Heart</topic><topic>Hematocrit</topic><topic>Heterocyclic Compounds, 2-Ring - pharmacology</topic><topic>Heterocyclic Compounds, 2-Ring - therapeutic use</topic><topic>Hypertension</topic><topic>Hypertension, Pulmonary - complications</topic><topic>Hypertension, Pulmonary - enzymology</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - pathology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>Hypertension, Pulmonary - prevention & control</topic><topic>Hypertrophy</topic><topic>Hypertrophy, Right Ventricular - enzymology</topic><topic>Hypertrophy, Right Ventricular - etiology</topic><topic>Hypertrophy, Right Ventricular - prevention & control</topic><topic>Hypoxia</topic><topic>Hypoxia - complications</topic><topic>Hypoxia - drug therapy</topic><topic>Hypoxia - enzymology</topic><topic>Hypoxia - pathology</topic><topic>Hypoxia - physiopathology</topic><topic>Inhibitor drugs</topic><topic>Inhibitors</topic><topic>Light microscopy</topic><topic>Lung - blood supply</topic><topic>Lung - drug effects</topic><topic>Lung - enzymology</topic><topic>Lung - pathology</topic><topic>Male</topic><topic>Nitric oxide</topic><topic>Nitric Oxide Synthase Type II - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Optical microscopy</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Pulmonary arteries</topic><topic>Pulmonary artery</topic><topic>Pulmonary Artery - drug effects</topic><topic>Pulmonary Artery - pathology</topic><topic>Pulmonary Artery - physiopathology</topic><topic>Pulmonary hypertension</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Time Factors</topic><topic>Veins & arteries</topic><topic>Ventricle</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Bao Hua</creatorcontrib><creatorcontrib>Maruyama, Junko</creatorcontrib><creatorcontrib>Yokochi, Ayumu</creatorcontrib><creatorcontrib>Mitani, Yoshihide</creatorcontrib><creatorcontrib>Maruyama, Kazuo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nursing & Allied Health Database</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Lung</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Bao Hua</au><au>Maruyama, Junko</au><au>Yokochi, Ayumu</au><au>Mitani, Yoshihide</au><au>Maruyama, Kazuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A novel inhibitor of inducible nitric oxide synthase, ONO-1714, does not ameliorate hypoxia-induced pulmonary hypertension in rats</atitle><jtitle>Lung</jtitle><addtitle>Lung</addtitle><date>2007-09-01</date><risdate>2007</risdate><volume>185</volume><issue>5</issue><spage>303</spage><epage>308</epage><pages>303-308</pages><issn>0341-2040</issn><eissn>1432-1750</eissn><coden>LUNGD9</coden><abstract>A recent study showed that long-term administration of the inducible nitric oxide synthase (iNOS) inhibitor L-NIL reduced the development of pulmonary hypertension. The purpose of the present study was to identify the effect of an another iNOS inhibitor, ONO-1714, on the development of pulmonary hypertensive vascular changes in chronic hypoxic pulmonary hypertension in rats. ONO-1714 was administered to rats exposed to hypobaric hypoxia (air at 380 mmHg) for 10 days. Muscularization of normally nonmuscular peripheral arteries and medial hypertrophy of normally muscular arteries were assessed by light microscopy. iNOS mRNA and protein levels of the lung were assessed in normal and hypoxic rats. Chronic hypoxia induced pulmonary hypertension, right ventricular hypertrophy, and hypertensive pulmonary vascular changes. Although an acute single injection of ONO-1714 induced a significant increase in mean pulmonary artery pressure in chronic hypoxic pulmonary hypertensive rats, the increase was slight and transient. There were no significant differences among rats with and without long-term administration of ONO-1714 in pulmonary artery pressure, right ventricular hypertrophy, medial wall thickness of muscular arteries, and the percentage of muscularized arteries at the alveolar wall and duct levels. Although there was a significantly increased expression of iNOS as assessed with the reverse-transcription polymerase chain reaction in rats that were exposed to 10 days of hypobaric hypoxia, we could not detect a significant level of iNOS protein by Western blotting. ONO-1714 does not have a therapeutic role in preventing the development of chronic hypoxic pulmonary hypertension.</abstract><cop>United States</cop><pub>Springer</pub><pmid>17721804</pmid><doi>10.1007/s00408-007-9024-z</doi><tpages>6</tpages></addata></record> |
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| ispartof | Lung, 2007-09, Vol.185 (5), p.303-308 |
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| subjects | Alveoli Amidines - pharmacology Amidines - therapeutic use Animals Antihypertensive Agents - pharmacology Antihypertensive Agents - therapeutic use Arteries Blood Pressure - drug effects Blotting, Western Body Weight - drug effects Chemical inhibitors Complications and side effects Disease Models, Animal Dosage and administration Drug therapy Enzyme Inhibitors - pharmacology Enzyme Inhibitors - therapeutic use Heart Hematocrit Heterocyclic Compounds, 2-Ring - pharmacology Heterocyclic Compounds, 2-Ring - therapeutic use Hypertension Hypertension, Pulmonary - complications Hypertension, Pulmonary - enzymology Hypertension, Pulmonary - etiology Hypertension, Pulmonary - pathology Hypertension, Pulmonary - physiopathology Hypertension, Pulmonary - prevention & control Hypertrophy Hypertrophy, Right Ventricular - enzymology Hypertrophy, Right Ventricular - etiology Hypertrophy, Right Ventricular - prevention & control Hypoxia Hypoxia - complications Hypoxia - drug therapy Hypoxia - enzymology Hypoxia - pathology Hypoxia - physiopathology Inhibitor drugs Inhibitors Light microscopy Lung - blood supply Lung - drug effects Lung - enzymology Lung - pathology Male Nitric oxide Nitric Oxide Synthase Type II - antagonists & inhibitors Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Nitric-oxide synthase Optical microscopy Polymerase chain reaction Proteins Pulmonary arteries Pulmonary artery Pulmonary Artery - drug effects Pulmonary Artery - pathology Pulmonary Artery - physiopathology Pulmonary hypertension Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Rodents Time Factors Veins & arteries Ventricle Western blotting |
| title | A novel inhibitor of inducible nitric oxide synthase, ONO-1714, does not ameliorate hypoxia-induced pulmonary hypertension in rats |
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