Oxidative stress in white coat hypertension; role of paraoxonase
Oxidative stress in sustained hypertension was shown with several biochemical parameters. Oxidized low-density lipoprotein (oxLDL) plays an important role during the atherosclerosis process and paraoxonase (PON1) can significantly inhibit lipid peroxidation. Serum PON1 activity, oxLDL and malondiald...
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| Veröffentlicht in: | Journal of human hypertension 2004-07, Vol.18 (7), p.523-528 |
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| creator | Uzun, H Karter, Y Aydin, S Çurgunlu, A Şimşek, G Yücel, R Vehiyd, S Ertürk, N Kutlu, A Benian, A Yaldiran, A Öztürk, E Erdine, S |
| description | Oxidative stress in sustained hypertension was shown with several biochemical parameters. Oxidized low-density lipoprotein (oxLDL) plays an important role during the atherosclerosis process and paraoxonase (PON1) can significantly inhibit lipid peroxidation. Serum PON1 activity, oxLDL and malondialdehyde (MDA) concentrations and their relationship with serum lipid parameters and systolic and diastolic blood pressures (SBP and DBP) were determined in subjects with white coat hypertension (WCH), sustained hypertension (HT) and normotension (NT). The study group consisted of a total of 86 subjects, 30 with WCH (14 male, 16 female subjects), 30 with HT (13 male, 17 female subjects) and 26 with NT (12 male, 14 female subjects). Both white coat hypertensive and hypertensive subjects had significantly higher levels of MDA than normotensives (
P |
| doi_str_mv | 10.1038/sj.jhh.1001697 |
| format | Article |
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P
<0.026 and
P
<0.001, respectively). The oxLDL level of the HT group was significantly higher than the NT group (
P
<0.023). The WCH group had an oxLDL level similar to both hypertensive and normotensive groups. HT and WCH groups had significantly lower PON1 levels than the normotensive group (
P
<0.001). oxLDL correlated with MDA positively (
P
=0.008), and PON1 negatively (
P
=0.008). A negative correlation between MDA and PON1 (
P
=0.014) was detected. MDA correlated positively with both SBP and DBP (
P
=0.001), while PON1 correlated with both of them negatively (
P
=0.01 and
P
=0.008, respectively). OxLDL correlated with diastolic blood pressure positively (
P
=0.008). Our data demonstrate that oxidative stress increase in WCH is associated with a decrease in PON1 activity. The reduction in PON1 activity may be one of the factors leading to an increase in oxidative status in WCH.</description><identifier>ISSN: 0950-9240</identifier><identifier>EISSN: 1476-5527</identifier><identifier>DOI: 10.1038/sj.jhh.1001697</identifier><identifier>PMID: 14985779</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adult ; Arterial hypertension. Arterial hypotension ; Arteriosclerosis ; Aryldialkylphosphatase - blood ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Blood Pressure Determination - adverse effects ; Cardiology. Vascular system ; Case-Control Studies ; Control ; Diastole ; Epidemiology ; Female ; Genetic aspects ; Genetic polymorphisms ; Health Administration ; Humans ; Hypertension ; Hypertension - blood ; Hypertension - etiology ; Hypertension - physiopathology ; Lipid peroxidation ; Lipoproteins, LDL - blood ; Male ; Malondialdehyde ; Malondialdehyde - blood ; Medical sciences ; Medicine ; Medicine & Public Health ; Middle Aged ; Office Visits ; original-article ; Oxidative Stress ; Paraoxonase ; Physiological aspects ; Public Health ; Risk factors ; Systole</subject><ispartof>Journal of human hypertension, 2004-07, Vol.18 (7), p.523-528</ispartof><rights>Springer Nature Limited 2004</rights><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2004</rights><rights>Nature Publishing Group 2004.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-9822bec2af254118f4bb30406a6829c88ba88304422594c71ad545249cae128c3</citedby><cites>FETCH-LOGICAL-c580t-9822bec2af254118f4bb30406a6829c88ba88304422594c71ad545249cae128c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.jhh.1001697$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.jhh.1001697$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15915859$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14985779$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Uzun, H</creatorcontrib><creatorcontrib>Karter, Y</creatorcontrib><creatorcontrib>Aydin, S</creatorcontrib><creatorcontrib>Çurgunlu, A</creatorcontrib><creatorcontrib>Şimşek, G</creatorcontrib><creatorcontrib>Yücel, R</creatorcontrib><creatorcontrib>Vehiyd, S</creatorcontrib><creatorcontrib>Ertürk, N</creatorcontrib><creatorcontrib>Kutlu, A</creatorcontrib><creatorcontrib>Benian, A</creatorcontrib><creatorcontrib>Yaldiran, A</creatorcontrib><creatorcontrib>Öztürk, E</creatorcontrib><creatorcontrib>Erdine, S</creatorcontrib><title>Oxidative stress in white coat hypertension; role of paraoxonase</title><title>Journal of human hypertension</title><addtitle>J Hum Hypertens</addtitle><addtitle>J Hum Hypertens</addtitle><description>Oxidative stress in sustained hypertension was shown with several biochemical parameters. Oxidized low-density lipoprotein (oxLDL) plays an important role during the atherosclerosis process and paraoxonase (PON1) can significantly inhibit lipid peroxidation. Serum PON1 activity, oxLDL and malondialdehyde (MDA) concentrations and their relationship with serum lipid parameters and systolic and diastolic blood pressures (SBP and DBP) were determined in subjects with white coat hypertension (WCH), sustained hypertension (HT) and normotension (NT). The study group consisted of a total of 86 subjects, 30 with WCH (14 male, 16 female subjects), 30 with HT (13 male, 17 female subjects) and 26 with NT (12 male, 14 female subjects). Both white coat hypertensive and hypertensive subjects had significantly higher levels of MDA than normotensives (
P
<0.026 and
P
<0.001, respectively). The oxLDL level of the HT group was significantly higher than the NT group (
P
<0.023). The WCH group had an oxLDL level similar to both hypertensive and normotensive groups. HT and WCH groups had significantly lower PON1 levels than the normotensive group (
P
<0.001). oxLDL correlated with MDA positively (
P
=0.008), and PON1 negatively (
P
=0.008). A negative correlation between MDA and PON1 (
P
=0.014) was detected. MDA correlated positively with both SBP and DBP (
P
=0.001), while PON1 correlated with both of them negatively (
P
=0.01 and
P
=0.008, respectively). OxLDL correlated with diastolic blood pressure positively (
P
=0.008). Our data demonstrate that oxidative stress increase in WCH is associated with a decrease in PON1 activity. The reduction in PON1 activity may be one of the factors leading to an increase in oxidative status in WCH.</description><subject>Adult</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Arteriosclerosis</subject><subject>Aryldialkylphosphatase - blood</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Blood Pressure Determination - adverse effects</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Control</subject><subject>Diastole</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Health Administration</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - blood</subject><subject>Hypertension - etiology</subject><subject>Hypertension - physiopathology</subject><subject>Lipid peroxidation</subject><subject>Lipoproteins, LDL - blood</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - blood</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Office Visits</subject><subject>original-article</subject><subject>Oxidative Stress</subject><subject>Paraoxonase</subject><subject>Physiological aspects</subject><subject>Public Health</subject><subject>Risk factors</subject><subject>Systole</subject><issn>0950-9240</issn><issn>1476-5527</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU1v1DAQhi0EokvhyhFFIHrL1nZsxxYXqoovqVIvcLYc76TxKmsvngTaf49XjbSAWvlga-aZd8bzEvKa0TWjjT7H7Xo7DOVNmTLtE7JiolW1lLx9SlbUSFobLugJeYG4LUxJ6ufkhAmjZduaFfl4fRs2bgq_oMIpA2IVYvV7CBNUPrmpGu72kCeIGFL8UOU0QpX6au-yS7cpOoSX5FnvRoRXy31Kfnz-9P3ya311_eXb5cVV7aWmU2005x147nouBWO6F13XUEGVU5obr3XntC4Bwbk0wrfMbaSQXBjvgHHtm1Nydq-7z-nnDDjZXUAP4-gipBmtUkoqw3UB3_0HbtOcY5nNciWoVKrltFBvH6WYMYq1hh-lbtwINsQ-Tdn5Q197wXTTFD11oNYPUOVsYBd8itCHEv-n4OyvggHcOA2YxnkqO8YHlX1OiBl6u89h5_KdZdQe7Le4tcV-u9hfCt4sv5q7HWyO-OJ3Ad4vgEPvxj676AMeOWmY1PLAnd9zWFLxBvJxPY-0_gMyKMOE</recordid><startdate>20040701</startdate><enddate>20040701</enddate><creator>Uzun, H</creator><creator>Karter, Y</creator><creator>Aydin, S</creator><creator>Çurgunlu, A</creator><creator>Şimşek, G</creator><creator>Yücel, R</creator><creator>Vehiyd, S</creator><creator>Ertürk, N</creator><creator>Kutlu, A</creator><creator>Benian, A</creator><creator>Yaldiran, A</creator><creator>Öztürk, E</creator><creator>Erdine, S</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20040701</creationdate><title>Oxidative stress in white coat hypertension; role of paraoxonase</title><author>Uzun, H ; Karter, Y ; Aydin, S ; Çurgunlu, A ; Şimşek, G ; Yücel, R ; Vehiyd, S ; Ertürk, N ; Kutlu, A ; Benian, A ; Yaldiran, A ; Öztürk, E ; Erdine, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c580t-9822bec2af254118f4bb30406a6829c88ba88304422594c71ad545249cae128c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Arteriosclerosis</topic><topic>Aryldialkylphosphatase - blood</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Blood Pressure Determination - adverse effects</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Control</topic><topic>Diastole</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Health Administration</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - blood</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>Lipid peroxidation</topic><topic>Lipoproteins, LDL - blood</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - blood</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Office Visits</topic><topic>original-article</topic><topic>Oxidative Stress</topic><topic>Paraoxonase</topic><topic>Physiological aspects</topic><topic>Public Health</topic><topic>Risk factors</topic><topic>Systole</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Uzun, H</creatorcontrib><creatorcontrib>Karter, Y</creatorcontrib><creatorcontrib>Aydin, S</creatorcontrib><creatorcontrib>Çurgunlu, A</creatorcontrib><creatorcontrib>Şimşek, G</creatorcontrib><creatorcontrib>Yücel, R</creatorcontrib><creatorcontrib>Vehiyd, S</creatorcontrib><creatorcontrib>Ertürk, N</creatorcontrib><creatorcontrib>Kutlu, A</creatorcontrib><creatorcontrib>Benian, A</creatorcontrib><creatorcontrib>Yaldiran, A</creatorcontrib><creatorcontrib>Öztürk, E</creatorcontrib><creatorcontrib>Erdine, S</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>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of human hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Uzun, H</au><au>Karter, Y</au><au>Aydin, S</au><au>Çurgunlu, A</au><au>Şimşek, G</au><au>Yücel, R</au><au>Vehiyd, S</au><au>Ertürk, N</au><au>Kutlu, A</au><au>Benian, A</au><au>Yaldiran, A</au><au>Öztürk, E</au><au>Erdine, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress in white coat hypertension; role of paraoxonase</atitle><jtitle>Journal of human hypertension</jtitle><stitle>J Hum Hypertens</stitle><addtitle>J Hum Hypertens</addtitle><date>2004-07-01</date><risdate>2004</risdate><volume>18</volume><issue>7</issue><spage>523</spage><epage>528</epage><pages>523-528</pages><issn>0950-9240</issn><eissn>1476-5527</eissn><abstract>Oxidative stress in sustained hypertension was shown with several biochemical parameters. Oxidized low-density lipoprotein (oxLDL) plays an important role during the atherosclerosis process and paraoxonase (PON1) can significantly inhibit lipid peroxidation. Serum PON1 activity, oxLDL and malondialdehyde (MDA) concentrations and their relationship with serum lipid parameters and systolic and diastolic blood pressures (SBP and DBP) were determined in subjects with white coat hypertension (WCH), sustained hypertension (HT) and normotension (NT). The study group consisted of a total of 86 subjects, 30 with WCH (14 male, 16 female subjects), 30 with HT (13 male, 17 female subjects) and 26 with NT (12 male, 14 female subjects). Both white coat hypertensive and hypertensive subjects had significantly higher levels of MDA than normotensives (
P
<0.026 and
P
<0.001, respectively). The oxLDL level of the HT group was significantly higher than the NT group (
P
<0.023). The WCH group had an oxLDL level similar to both hypertensive and normotensive groups. HT and WCH groups had significantly lower PON1 levels than the normotensive group (
P
<0.001). oxLDL correlated with MDA positively (
P
=0.008), and PON1 negatively (
P
=0.008). A negative correlation between MDA and PON1 (
P
=0.014) was detected. MDA correlated positively with both SBP and DBP (
P
=0.001), while PON1 correlated with both of them negatively (
P
=0.01 and
P
=0.008, respectively). OxLDL correlated with diastolic blood pressure positively (
P
=0.008). Our data demonstrate that oxidative stress increase in WCH is associated with a decrease in PON1 activity. The reduction in PON1 activity may be one of the factors leading to an increase in oxidative status in WCH.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>14985779</pmid><doi>10.1038/sj.jhh.1001697</doi><tpages>6</tpages></addata></record> |
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| ispartof | Journal of human hypertension, 2004-07, Vol.18 (7), p.523-528 |
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| language | eng |
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| source | MEDLINE; SpringerLink; EZB Electronic Journals Library |
| subjects | Adult Arterial hypertension. Arterial hypotension Arteriosclerosis Aryldialkylphosphatase - blood Biological and medical sciences Blood and lymphatic vessels Blood Pressure Blood Pressure Determination - adverse effects Cardiology. Vascular system Case-Control Studies Control Diastole Epidemiology Female Genetic aspects Genetic polymorphisms Health Administration Humans Hypertension Hypertension - blood Hypertension - etiology Hypertension - physiopathology Lipid peroxidation Lipoproteins, LDL - blood Male Malondialdehyde Malondialdehyde - blood Medical sciences Medicine Medicine & Public Health Middle Aged Office Visits original-article Oxidative Stress Paraoxonase Physiological aspects Public Health Risk factors Systole |
| title | Oxidative stress in white coat hypertension; role of paraoxonase |
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