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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Veröffentlicht in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2005-12, Vol.46 (6), p.1355-1361
Hauptverfasser: Sun, Ying, Carretero, Oscar A, Xu, Jiang, Rhaleb, Nour-Eddine, Wang, Fangfei, Lin, Chunxia, Yang, James J, Pagano, Patrick J, Yang, Xiao-Ping
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container_end_page 1361
container_issue 6
container_start_page 1355
container_title Hypertension (Dallas, Tex. 1979)
container_volume 46
creator Sun, Ying
Carretero, Oscar A
Xu, Jiang
Rhaleb, Nour-Eddine
Wang, Fangfei
Lin, Chunxia
Yang, James J
Pagano, Patrick J
Yang, Xiao-Ping
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><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 &amp; 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 &amp; 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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source MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals; Journals@Ovid Complete
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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