Chronic Hydroxychloroquine Improves Endothelial Dysfunction and Protects Kidney in a Mouse Model of Systemic Lupus Erythematosus
Hydroxychloroquine has been shown to be efficacious in the treatment of autoimmune diseases, including systemic lupus erythematosus. Hydroxychloroquine-treated lupus patients showed a lower incidence of thromboembolic disease. Endothelial dysfunction, the earliest indicator of the development of car...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2014-08, Vol.64 (2), p.330-337 |
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| creator | Gómez-Guzmán, Manuel Jiménez, Rosario Romero, Miguel Sánchez, Manuel Zarzuelo, María José Gómez-Morales, Mercedes O’Valle, Francisco López-Farré, Antonio José Algieri, Francesca Gálvez, Julio Pérez-Vizcaino, Francisco Sabio, José Mario Duarte, Juan |
| description | Hydroxychloroquine has been shown to be efficacious in the treatment of autoimmune diseases, including systemic lupus erythematosus. Hydroxychloroquine-treated lupus patients showed a lower incidence of thromboembolic disease. Endothelial dysfunction, the earliest indicator of the development of cardiovascular disease, is present in lupus. Whether hydroxychloroquine improves endothelial function in lupus is not clear. The aim of this study was to analyze the effects of hydroxychloroquine on hypertension, endothelial dysfunction, and renal injury in a female mouse model of lupus. NZBWF1 (lupus) and NZW/LacJ (control) mice were treated with hydroxychloroquine 10 mg/kg per day by oral gavage, or with tempol and apocynin in the drinking water, for 5 weeks. Hydroxychloroquine treatment did not alter lupus disease activity (assessed by plasma double-stranded DNA autoantibodies) but prevented hypertension, cardiac and renal hypertrophy, proteinuria, and renal injury in lupus mice. Aortae from lupus mice showed reduced endothelium-dependent vasodilator responses to acetylcholine and enhanced contraction to phenylephrine, which were normalized by hydroxychloroquine or antioxidant treatments. No differences among all experimental groups were found in both the relaxant responses to acetylcholine and the contractile responses to phenylephrine in rings incubated with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester. Vascular reactive oxygen species content and mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase subunits NOX-1 and p47 were increased in lupus mice and reduced by hydroxychloroquine or antioxidants. Chronic hydroxychloroquine treatment reduced hypertension, endothelial dysfunction, and organ damage in severe lupus mice, despite the persistent elevation of anti–double-stranded DNA, suggesting the involvement of new additional mechanisms to improve cardiovascular complications. |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.114.03587 |
| format | Article |
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Hydroxychloroquine-treated lupus patients showed a lower incidence of thromboembolic disease. Endothelial dysfunction, the earliest indicator of the development of cardiovascular disease, is present in lupus. Whether hydroxychloroquine improves endothelial function in lupus is not clear. The aim of this study was to analyze the effects of hydroxychloroquine on hypertension, endothelial dysfunction, and renal injury in a female mouse model of lupus. NZBWF1 (lupus) and NZW/LacJ (control) mice were treated with hydroxychloroquine 10 mg/kg per day by oral gavage, or with tempol and apocynin in the drinking water, for 5 weeks. Hydroxychloroquine treatment did not alter lupus disease activity (assessed by plasma double-stranded DNA autoantibodies) but prevented hypertension, cardiac and renal hypertrophy, proteinuria, and renal injury in lupus mice. Aortae from lupus mice showed reduced endothelium-dependent vasodilator responses to acetylcholine and enhanced contraction to phenylephrine, which were normalized by hydroxychloroquine or antioxidant treatments. No differences among all experimental groups were found in both the relaxant responses to acetylcholine and the contractile responses to phenylephrine in rings incubated with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester. Vascular reactive oxygen species content and mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase subunits NOX-1 and p47 were increased in lupus mice and reduced by hydroxychloroquine or antioxidants. Chronic hydroxychloroquine treatment reduced hypertension, endothelial dysfunction, and organ damage in severe lupus mice, despite the persistent elevation of anti–double-stranded DNA, suggesting the involvement of new additional mechanisms to improve cardiovascular complications.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.114.03587</identifier><identifier>PMID: 24842914</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Acute Kidney Injury - drug therapy ; Acute Kidney Injury - physiopathology ; Acute Kidney Injury - prevention & control ; Animals ; Antibiotics. Antiinfectious agents. Antiparasitic agents ; Antiparasitic agents ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Cardiology. Vascular system ; Disease Models, Animal ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiopathology ; Enzyme Inhibitors - pharmacology ; Enzyme Inhibitors - therapeutic use ; Female ; Hydroxychloroquine - pharmacology ; Hydroxychloroquine - therapeutic use ; Hypertension - complications ; Hypertension - drug therapy ; Hypertension - physiopathology ; Kidney - drug effects ; Kidney - physiopathology ; Kidneys ; Lupus Erythematosus, Systemic - complications ; Lupus Erythematosus, Systemic - drug therapy ; Lupus Erythematosus, Systemic - physiopathology ; Medical sciences ; Mice ; Nephrology. Urinary tract diseases ; Pharmacology. Drug treatments ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Urinary system involvement in other diseases. Miscellaneous</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2014-08, Vol.64 (2), p.330-337</ispartof><rights>2014 American Heart Association, Inc</rights><rights>2015 INIST-CNRS</rights><rights>2014 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6447-73e791f5d7dded9e121753cba13c8e278120aa2fb3680464ef0f478bad1aa1e3</citedby><cites>FETCH-LOGICAL-c6447-73e791f5d7dded9e121753cba13c8e278120aa2fb3680464ef0f478bad1aa1e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3688,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28610649$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24842914$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gómez-Guzmán, Manuel</creatorcontrib><creatorcontrib>Jiménez, Rosario</creatorcontrib><creatorcontrib>Romero, Miguel</creatorcontrib><creatorcontrib>Sánchez, Manuel</creatorcontrib><creatorcontrib>Zarzuelo, María José</creatorcontrib><creatorcontrib>Gómez-Morales, Mercedes</creatorcontrib><creatorcontrib>O’Valle, Francisco</creatorcontrib><creatorcontrib>López-Farré, Antonio José</creatorcontrib><creatorcontrib>Algieri, Francesca</creatorcontrib><creatorcontrib>Gálvez, Julio</creatorcontrib><creatorcontrib>Pérez-Vizcaino, Francisco</creatorcontrib><creatorcontrib>Sabio, José Mario</creatorcontrib><creatorcontrib>Duarte, Juan</creatorcontrib><title>Chronic Hydroxychloroquine Improves Endothelial Dysfunction and Protects Kidney in a Mouse Model of Systemic Lupus Erythematosus</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Hydroxychloroquine has been shown to be efficacious in the treatment of autoimmune diseases, including systemic lupus erythematosus. Hydroxychloroquine-treated lupus patients showed a lower incidence of thromboembolic disease. Endothelial dysfunction, the earliest indicator of the development of cardiovascular disease, is present in lupus. Whether hydroxychloroquine improves endothelial function in lupus is not clear. The aim of this study was to analyze the effects of hydroxychloroquine on hypertension, endothelial dysfunction, and renal injury in a female mouse model of lupus. NZBWF1 (lupus) and NZW/LacJ (control) mice were treated with hydroxychloroquine 10 mg/kg per day by oral gavage, or with tempol and apocynin in the drinking water, for 5 weeks. Hydroxychloroquine treatment did not alter lupus disease activity (assessed by plasma double-stranded DNA autoantibodies) but prevented hypertension, cardiac and renal hypertrophy, proteinuria, and renal injury in lupus mice. Aortae from lupus mice showed reduced endothelium-dependent vasodilator responses to acetylcholine and enhanced contraction to phenylephrine, which were normalized by hydroxychloroquine or antioxidant treatments. No differences among all experimental groups were found in both the relaxant responses to acetylcholine and the contractile responses to phenylephrine in rings incubated with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester. Vascular reactive oxygen species content and mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase subunits NOX-1 and p47 were increased in lupus mice and reduced by hydroxychloroquine or antioxidants. Chronic hydroxychloroquine treatment reduced hypertension, endothelial dysfunction, and organ damage in severe lupus mice, despite the persistent elevation of anti–double-stranded DNA, suggesting the involvement of new additional mechanisms to improve cardiovascular complications.</description><subject>Acute Kidney Injury - drug therapy</subject><subject>Acute Kidney Injury - physiopathology</subject><subject>Acute Kidney Injury - prevention & control</subject><subject>Animals</subject><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>Antiparasitic agents</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Disease Models, Animal</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Female</subject><subject>Hydroxychloroquine - pharmacology</subject><subject>Hydroxychloroquine - therapeutic use</subject><subject>Hypertension - complications</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Kidney - drug effects</subject><subject>Kidney - physiopathology</subject><subject>Kidneys</subject><subject>Lupus Erythematosus, Systemic - complications</subject><subject>Lupus Erythematosus, Systemic - drug therapy</subject><subject>Lupus Erythematosus, Systemic - physiopathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Pharmacology. Drug treatments</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Urinary system involvement in other diseases. Miscellaneous</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE9vEzEQxS0EoqHwFZA5IPWyxbP2_jtwiEIgUUNb0RzgtHLsWe2C1w72bsve-Oi4TQCJExdbGv3mvTePkFfAzgFyeLP6cr38tF1e3qyvLuereRyKc8azsnhEZpClIhFZzh-TGYNKJBXA5xPyLISvjIEQonhKTlJRirQCMSM_F613tlN0NWnvfkyqNc6772Nnka77vXe3GOjSaje0aDpp6LspNKNVQ-cslVbTa-8GVEOgF522ONEujulHNwaMr0ZDXUNvpjBgH002436Mcn6Kar0cXBjDc_KkkSbgi-N_Srbvl9vFKtlcfVgv5ptE5TFzUnAsKmgyXWiNukJIoci42kngqsS0KCFlUqbNjuclE7nAhjWiKHdSg5SA_JScHWT399dhGOq-CwqNkRZj2Bqy6MLLNOMRrQ6o8i4Ej029910v_VQDq-_7r__pPw5F_dB_3H15tBl3Peo_m78Lj8DrIyCDkqbx0qou_OXKHFguqsi9PXB3zgzowzcz3qGvW5RmaP8jyC-lI6bH</recordid><startdate>201408</startdate><enddate>201408</enddate><creator>Gómez-Guzmán, Manuel</creator><creator>Jiménez, Rosario</creator><creator>Romero, Miguel</creator><creator>Sánchez, Manuel</creator><creator>Zarzuelo, María José</creator><creator>Gómez-Morales, Mercedes</creator><creator>O’Valle, Francisco</creator><creator>López-Farré, Antonio José</creator><creator>Algieri, Francesca</creator><creator>Gálvez, Julio</creator><creator>Pérez-Vizcaino, Francisco</creator><creator>Sabio, José Mario</creator><creator>Duarte, Juan</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</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>201408</creationdate><title>Chronic Hydroxychloroquine Improves Endothelial Dysfunction and Protects Kidney in a Mouse Model of Systemic Lupus Erythematosus</title><author>Gómez-Guzmán, Manuel ; Jiménez, Rosario ; Romero, Miguel ; Sánchez, Manuel ; Zarzuelo, María José ; Gómez-Morales, Mercedes ; O’Valle, Francisco ; López-Farré, Antonio José ; Algieri, Francesca ; Gálvez, Julio ; Pérez-Vizcaino, Francisco ; Sabio, José Mario ; Duarte, Juan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6447-73e791f5d7dded9e121753cba13c8e278120aa2fb3680464ef0f478bad1aa1e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acute Kidney Injury - drug therapy</topic><topic>Acute Kidney Injury - physiopathology</topic><topic>Acute Kidney Injury - prevention & control</topic><topic>Animals</topic><topic>Antibiotics. Antiinfectious agents. Antiparasitic agents</topic><topic>Antiparasitic agents</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Disease Models, Animal</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Female</topic><topic>Hydroxychloroquine - pharmacology</topic><topic>Hydroxychloroquine - therapeutic use</topic><topic>Hypertension - complications</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - physiopathology</topic><topic>Kidney - drug effects</topic><topic>Kidney - physiopathology</topic><topic>Kidneys</topic><topic>Lupus Erythematosus, Systemic - complications</topic><topic>Lupus Erythematosus, Systemic - drug therapy</topic><topic>Lupus Erythematosus, Systemic - physiopathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Pharmacology. Drug treatments</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. 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Hydroxychloroquine-treated lupus patients showed a lower incidence of thromboembolic disease. Endothelial dysfunction, the earliest indicator of the development of cardiovascular disease, is present in lupus. Whether hydroxychloroquine improves endothelial function in lupus is not clear. The aim of this study was to analyze the effects of hydroxychloroquine on hypertension, endothelial dysfunction, and renal injury in a female mouse model of lupus. NZBWF1 (lupus) and NZW/LacJ (control) mice were treated with hydroxychloroquine 10 mg/kg per day by oral gavage, or with tempol and apocynin in the drinking water, for 5 weeks. Hydroxychloroquine treatment did not alter lupus disease activity (assessed by plasma double-stranded DNA autoantibodies) but prevented hypertension, cardiac and renal hypertrophy, proteinuria, and renal injury in lupus mice. Aortae from lupus mice showed reduced endothelium-dependent vasodilator responses to acetylcholine and enhanced contraction to phenylephrine, which were normalized by hydroxychloroquine or antioxidant treatments. No differences among all experimental groups were found in both the relaxant responses to acetylcholine and the contractile responses to phenylephrine in rings incubated with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester. Vascular reactive oxygen species content and mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase subunits NOX-1 and p47 were increased in lupus mice and reduced by hydroxychloroquine or antioxidants. Chronic hydroxychloroquine treatment reduced hypertension, endothelial dysfunction, and organ damage in severe lupus mice, despite the persistent elevation of anti–double-stranded DNA, suggesting the involvement of new additional mechanisms to improve cardiovascular complications.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>24842914</pmid><doi>10.1161/HYPERTENSIONAHA.114.03587</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2014-08, Vol.64 (2), p.330-337 |
| issn | 0194-911X 1524-4563 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1544738253 |
| source | MEDLINE; American Heart Association; Journals@Ovid Complete; EZB Electronic Journals Library |
| subjects | Acute Kidney Injury - drug therapy Acute Kidney Injury - physiopathology Acute Kidney Injury - prevention & control Animals Antibiotics. Antiinfectious agents. Antiparasitic agents Antiparasitic agents Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure - drug effects Cardiology. Vascular system Disease Models, Animal Endothelium, Vascular - drug effects Endothelium, Vascular - physiopathology Enzyme Inhibitors - pharmacology Enzyme Inhibitors - therapeutic use Female Hydroxychloroquine - pharmacology Hydroxychloroquine - therapeutic use Hypertension - complications Hypertension - drug therapy Hypertension - physiopathology Kidney - drug effects Kidney - physiopathology Kidneys Lupus Erythematosus, Systemic - complications Lupus Erythematosus, Systemic - drug therapy Lupus Erythematosus, Systemic - physiopathology Medical sciences Mice Nephrology. Urinary tract diseases Pharmacology. Drug treatments Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Urinary system involvement in other diseases. Miscellaneous |
| title | Chronic Hydroxychloroquine Improves Endothelial Dysfunction and Protects Kidney in a Mouse Model of Systemic Lupus Erythematosus |
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