Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate–Salt Hypertension
Although NO derived from endothelial NO synthase (eNOS) is thought to be cardioprotective, the role of inducible NO synthase (iNOS) remains controversial. Using mice lacking iNOS (iNOS−/−), we studied (1) whether development of hypertension, cardiac hypertrophy, and dysfunction after deoxycorticoste...
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description | Although NO derived from endothelial NO synthase (eNOS) is thought to be cardioprotective, the role of inducible NO synthase (iNOS) remains controversial. Using mice lacking iNOS (iNOS−/−), we studied (1) whether development of hypertension, cardiac hypertrophy, and dysfunction after deoxycorticosterone acetate (DOCA)–salt would be less severe compared with wild-type controls (WT; C57BL/6J), and (2) whether the cardioprotection attributable to lack of iNOS is mediated by reduced oxidative stress. Mice were uninephrectomized and received either DOCA-salt (30 mg/mouse SC and 1% NaCl+0.2% KCl in drinking water) or vehicle (tap water) for 12 weeks. Systolic blood pressure (SBP) was measured weekly. Left ventricular (LV) ejection fraction (EF) by echocardiography and cardiac response to isoproterenol (50 ng/mouse IV) were studied at the end of the experiment. Expression of eNOS and iNOS as well as the oxidative stress markers 4-hydroxy-2-nonenal (4-HNE, a marker of lipid peroxidation) and nitrotyrosine (a marker for peroxynitrite) were determined by Western blot and immunohistochemical staining, respectively. DOCA-salt increased SBP and LV weight similarly in both strains and decreased EF in WT but not in iNOS−/−. Cardiac contractile and relaxation responses to isoproterenol were greater, 4-HNE and nitrotyrosine levels were lower, and eNOS expression tended to be higher in iNOS−/−. We conclude that lack of iNOS leads to better preservation of cardiac function, which may be mediated by reduced oxidative stress and increased eNOS; however, it does not seem to play a significant role in preventing DOCA-salt–induced hypertension and hypertrophy. |
doi_str_mv | 10.1161/01.HYP.0000192651.06674.3f |
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Using mice lacking iNOS (iNOS−/−), we studied (1) whether development of hypertension, cardiac hypertrophy, and dysfunction after deoxycorticosterone acetate (DOCA)–salt would be less severe compared with wild-type controls (WT; C57BL/6J), and (2) whether the cardioprotection attributable to lack of iNOS is mediated by reduced oxidative stress. Mice were uninephrectomized and received either DOCA-salt (30 mg/mouse SC and 1% NaCl+0.2% KCl in drinking water) or vehicle (tap water) for 12 weeks. Systolic blood pressure (SBP) was measured weekly. Left ventricular (LV) ejection fraction (EF) by echocardiography and cardiac response to isoproterenol (50 ng/mouse IV) were studied at the end of the experiment. Expression of eNOS and iNOS as well as the oxidative stress markers 4-hydroxy-2-nonenal (4-HNE, a marker of lipid peroxidation) and nitrotyrosine (a marker for peroxynitrite) were determined by Western blot and immunohistochemical staining, respectively. DOCA-salt increased SBP and LV weight similarly in both strains and decreased EF in WT but not in iNOS−/−. Cardiac contractile and relaxation responses to isoproterenol were greater, 4-HNE and nitrotyrosine levels were lower, and eNOS expression tended to be higher in iNOS−/−. We conclude that lack of iNOS leads to better preservation of cardiac function, which may be mediated by reduced oxidative stress and increased eNOS; however, it does not seem to play a significant role in preventing DOCA-salt–induced hypertension and hypertrophy.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000192651.06674.3f</identifier><identifier>PMID: 16286571</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Aldehydes - metabolism ; Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Cardiology. Vascular system ; Cardiotonic Agents - pharmacology ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Desoxycorticosterone ; Experimental diseases ; Fundamental and applied biological sciences. Psychology ; Heart ; Heart - drug effects ; Heart - physiopathology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hemodynamics. Rheology ; Hypertension - chemically induced ; Hypertension - metabolism ; Hypertension - physiopathology ; Hypertrophy, Left Ventricular - chemically induced ; Isoproterenol - pharmacology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium - enzymology ; Nitric Oxide Synthase Type II - deficiency ; Nitric Oxide Synthase Type II - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Oxidative Stress ; Sodium Chloride ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism ; Vertebrates: cardiovascular system</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2005-12, Vol.46 (6), p.1355-1361</ispartof><rights>2005 American Heart Association, Inc.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4714-883a89066e09d63e0eb37e5c04232ac231334579a56ebb196d2f518fe418297c3</citedby><cites>FETCH-LOGICAL-c4714-883a89066e09d63e0eb37e5c04232ac231334579a56ebb196d2f518fe418297c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,782,786,887,3689,27931,27932</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17302403$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16286571$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Ying</creatorcontrib><creatorcontrib>Carretero, Oscar A</creatorcontrib><creatorcontrib>Xu, Jiang</creatorcontrib><creatorcontrib>Rhaleb, Nour-Eddine</creatorcontrib><creatorcontrib>Wang, Fangfei</creatorcontrib><creatorcontrib>Lin, Chunxia</creatorcontrib><creatorcontrib>Yang, James J</creatorcontrib><creatorcontrib>Pagano, Patrick J</creatorcontrib><creatorcontrib>Yang, Xiao-Ping</creatorcontrib><title>Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate–Salt Hypertension</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Although NO derived from endothelial NO synthase (eNOS) is thought to be cardioprotective, the role of inducible NO synthase (iNOS) remains controversial. Using mice lacking iNOS (iNOS−/−), we studied (1) whether development of hypertension, cardiac hypertrophy, and dysfunction after deoxycorticosterone acetate (DOCA)–salt would be less severe compared with wild-type controls (WT; C57BL/6J), and (2) whether the cardioprotection attributable to lack of iNOS is mediated by reduced oxidative stress. Mice were uninephrectomized and received either DOCA-salt (30 mg/mouse SC and 1% NaCl+0.2% KCl in drinking water) or vehicle (tap water) for 12 weeks. Systolic blood pressure (SBP) was measured weekly. Left ventricular (LV) ejection fraction (EF) by echocardiography and cardiac response to isoproterenol (50 ng/mouse IV) were studied at the end of the experiment. Expression of eNOS and iNOS as well as the oxidative stress markers 4-hydroxy-2-nonenal (4-HNE, a marker of lipid peroxidation) and nitrotyrosine (a marker for peroxynitrite) were determined by Western blot and immunohistochemical staining, respectively. DOCA-salt increased SBP and LV weight similarly in both strains and decreased EF in WT but not in iNOS−/−. Cardiac contractile and relaxation responses to isoproterenol were greater, 4-HNE and nitrotyrosine levels were lower, and eNOS expression tended to be higher in iNOS−/−. We conclude that lack of iNOS leads to better preservation of cardiac function, which may be mediated by reduced oxidative stress and increased eNOS; however, it does not seem to play a significant role in preventing DOCA-salt–induced hypertension and hypertrophy.</description><subject>Aldehydes - metabolism</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Desoxycorticosterone</subject><subject>Experimental diseases</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Hemodynamics. Rheology</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Hypertrophy, Left Ventricular - chemically induced</subject><subject>Isoproterenol - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myocardium - enzymology</subject><subject>Nitric Oxide Synthase Type II - deficiency</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Oxidative Stress</subject><subject>Sodium Chloride</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - metabolism</subject><subject>Vertebrates: cardiovascular system</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkd9u0zAUxiMEYmXwCshC4jLF_-IkXCBN3aCVCkUUBFxZjnNCzDI7st1tvds77A14NJ4Eb60oWLKP5PP7zpG-L8teEDwlRJBXmEzn3z9OcTqkpqIgUyxEyaese5BNSEF5zgvBHmaT1OZ5Tci3o-xJCD8TzjkvH2dHRNBKFCWZZL-WSp8j16GFbTfaNAOgDyu03trYqwDoE6RfCGh1bVoVzSWgdfQQAlK2RWe2V_auO1O-NUonOozOJll0aBHc6F0ED9YNyFj03mhAX03s0Sm46612PhrtQiKcBXSiIaoIv29u12qIaL4dwUewwTj7NHvUqSHAs309zr68Pfs8m-fL1bvF7GSZa14SnlcVU1WdnABct4IBhoaVUGjMKaNKU0YY40VZq0JA05BatLQrSNUBJxWtS82Osze7ueOmuYBWg41eDXL05kL5rXTKyP871vTyh7uUXGAicJEGvN4N0N6F4KH7qyVY3iUnMZEpOXlITt4nJ1mXxM__3X6Q7qNKwMs9oIJWQ-eT9yYcuJJhyjFLHN9xV25I5obzYXMFXvaQfO3vV3MqqpxiXJD04Dxdytkfuim2nw</recordid><startdate>200512</startdate><enddate>200512</enddate><creator>Sun, Ying</creator><creator>Carretero, Oscar A</creator><creator>Xu, Jiang</creator><creator>Rhaleb, Nour-Eddine</creator><creator>Wang, Fangfei</creator><creator>Lin, Chunxia</creator><creator>Yang, James J</creator><creator>Pagano, Patrick J</creator><creator>Yang, Xiao-Ping</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>5PM</scope></search><sort><creationdate>200512</creationdate><title>Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate–Salt Hypertension</title><author>Sun, Ying ; Carretero, Oscar A ; Xu, Jiang ; Rhaleb, Nour-Eddine ; Wang, Fangfei ; Lin, Chunxia ; Yang, James J ; Pagano, Patrick J ; Yang, Xiao-Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4714-883a89066e09d63e0eb37e5c04232ac231334579a56ebb196d2f518fe418297c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aldehydes - metabolism</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Cardiology. Vascular system</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Desoxycorticosterone</topic><topic>Experimental diseases</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Heart - physiopathology</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Hemodynamics. Rheology</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Hypertrophy, Left Ventricular - chemically induced</topic><topic>Isoproterenol - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myocardium - enzymology</topic><topic>Nitric Oxide Synthase Type II - deficiency</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Oxidative Stress</topic><topic>Sodium Chloride</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - metabolism</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Ying</creatorcontrib><creatorcontrib>Carretero, Oscar A</creatorcontrib><creatorcontrib>Xu, Jiang</creatorcontrib><creatorcontrib>Rhaleb, Nour-Eddine</creatorcontrib><creatorcontrib>Wang, Fangfei</creatorcontrib><creatorcontrib>Lin, Chunxia</creatorcontrib><creatorcontrib>Yang, James J</creatorcontrib><creatorcontrib>Pagano, Patrick J</creatorcontrib><creatorcontrib>Yang, Xiao-Ping</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>PubMed Central (Full Participant titles)</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Ying</au><au>Carretero, Oscar A</au><au>Xu, Jiang</au><au>Rhaleb, Nour-Eddine</au><au>Wang, Fangfei</au><au>Lin, Chunxia</au><au>Yang, James J</au><au>Pagano, Patrick J</au><au>Yang, Xiao-Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate–Salt Hypertension</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2005-12</date><risdate>2005</risdate><volume>46</volume><issue>6</issue><spage>1355</spage><epage>1361</epage><pages>1355-1361</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Although NO derived from endothelial NO synthase (eNOS) is thought to be cardioprotective, the role of inducible NO synthase (iNOS) remains controversial. Using mice lacking iNOS (iNOS−/−), we studied (1) whether development of hypertension, cardiac hypertrophy, and dysfunction after deoxycorticosterone acetate (DOCA)–salt would be less severe compared with wild-type controls (WT; C57BL/6J), and (2) whether the cardioprotection attributable to lack of iNOS is mediated by reduced oxidative stress. Mice were uninephrectomized and received either DOCA-salt (30 mg/mouse SC and 1% NaCl+0.2% KCl in drinking water) or vehicle (tap water) for 12 weeks. Systolic blood pressure (SBP) was measured weekly. Left ventricular (LV) ejection fraction (EF) by echocardiography and cardiac response to isoproterenol (50 ng/mouse IV) were studied at the end of the experiment. Expression of eNOS and iNOS as well as the oxidative stress markers 4-hydroxy-2-nonenal (4-HNE, a marker of lipid peroxidation) and nitrotyrosine (a marker for peroxynitrite) were determined by Western blot and immunohistochemical staining, respectively. DOCA-salt increased SBP and LV weight similarly in both strains and decreased EF in WT but not in iNOS−/−. Cardiac contractile and relaxation responses to isoproterenol were greater, 4-HNE and nitrotyrosine levels were lower, and eNOS expression tended to be higher in iNOS−/−. We conclude that lack of iNOS leads to better preservation of cardiac function, which may be mediated by reduced oxidative stress and increased eNOS; however, it does not seem to play a significant role in preventing DOCA-salt–induced hypertension and hypertrophy.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>16286571</pmid><doi>10.1161/01.HYP.0000192651.06674.3f</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aldehydes - metabolism Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure Cardiology. Vascular system Cardiotonic Agents - pharmacology Clinical manifestations. Epidemiology. Investigative techniques. Etiology Desoxycorticosterone Experimental diseases Fundamental and applied biological sciences. Psychology Heart Heart - drug effects Heart - physiopathology Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hemodynamics. Rheology Hypertension - chemically induced Hypertension - metabolism Hypertension - physiopathology Hypertrophy, Left Ventricular - chemically induced Isoproterenol - pharmacology Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Myocardium - enzymology Nitric Oxide Synthase Type II - deficiency Nitric Oxide Synthase Type II - metabolism Nitric Oxide Synthase Type III - metabolism Oxidative Stress Sodium Chloride Tyrosine - analogs & derivatives Tyrosine - metabolism Vertebrates: cardiovascular system |
title | Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate–Salt Hypertension |
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