Increased Oxidative Stress in Experimental Renovascular Hypertension
The pathophysiological mechanisms responsible for maintenance of chronic renovascular hypertension remain undefined. Excess angiotensin II generation may lead to release of reactive oxygen species and increased vasoconstrictor activity. To examine the potential involvement of oxidation-sensitive mec...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2001-02, Vol.37 (2, Part 2 Suppl), p.541-546 |
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| container_issue | 2, Part 2 Suppl |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Lerman, Lilach O Nath, Karl A Rodriguez-Porcel, Martin Krier, James D Schwartz, Robert S Napoli, Claudio Romero, J Carlos |
| description | The pathophysiological mechanisms responsible for maintenance of chronic renovascular hypertension remain undefined. Excess angiotensin II generation may lead to release of reactive oxygen species and increased vasoconstrictor activity. To examine the potential involvement of oxidation-sensitive mechanisms in the pathophysiology of renovascular hypertension, blood samples were collected and renal blood flow measured with electron-beam computed tomography in pigs 5 and 10 weeks after induction of unilateral renal artery stenosis (n=7) or sham operation (n=7). Five weeks after procedure, plasma renin activity and mean arterial pressure were elevated in hypertensive pigs. Levels of prostaglandin F2α (PGF2α)–isoprostanes, vasoconstrictors and markers of oxidative stress, also were significantly increased (157±21 versus 99±16 pg/mL;P |
| doi_str_mv | 10.1161/01.hyp.37.2.541 |
| format | Article |
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Excess angiotensin II generation may lead to release of reactive oxygen species and increased vasoconstrictor activity. To examine the potential involvement of oxidation-sensitive mechanisms in the pathophysiology of renovascular hypertension, blood samples were collected and renal blood flow measured with electron-beam computed tomography in pigs 5 and 10 weeks after induction of unilateral renal artery stenosis (n=7) or sham operation (n=7). Five weeks after procedure, plasma renin activity and mean arterial pressure were elevated in hypertensive pigs. Levels of prostaglandin F2α (PGF2α)–isoprostanes, vasoconstrictors and markers of oxidative stress, also were significantly increased (157±21 versus 99±16 pg/mL;P <0.05) and correlated with both plasma renin activity (r =0.83) and arterial pressure (r =0.82). By 10 weeks, plasma renin activity returned to baseline but arterial pressure remained elevated (144±10 versus 115±5 mm Hg;P <0.05). Isoprostane levels remained high and still correlated directly with the increase in arterial pressure (r =0.7) but not with plasma renin activity. Stenotic kidney blood flow was decreased at both studies. In shock-frozen cortical tissue, ex vivo endogenous intracellular radical scavengers were significantly decreased in both kidneys. The present study demonstrates, for the first time, that in early renovascular hypertension, an increase in plasma renin activity and arterial pressure is associated with increased systemic oxidative stress. When plasma renin activity later declines, PGF2α-isoprostanes remain elevated, possibly due to local activation or slow responses to angiotensin II, and may participate in sustenance of arterial pressure. Moreover, oxidation-sensitive mechanisms may influence ischemic and hypertensive parenchymal renal injury.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.37.2.541</identifier><identifier>PMID: 11230332</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Cardiology. Vascular system ; Dinoprost - analogs & derivatives ; Dinoprost - blood ; Experimental diseases ; F2-Isoprostanes ; Female ; Free Radical Scavengers - analysis ; Hypertension, Renovascular - blood ; Hypertension, Renovascular - etiology ; Hypertension, Renovascular - physiopathology ; Kidney Cortex - blood supply ; Kidney Cortex - metabolism ; Medical sciences ; Oxidative Stress ; Renal Artery Obstruction - complications ; Renal Circulation ; Renin - blood ; Swine ; Thiobarbituric Acid Reactive Substances - analysis</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2001-02, Vol.37 (2, Part 2 Suppl), p.541-546</ispartof><rights>2001 American Heart Association, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. 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Excess angiotensin II generation may lead to release of reactive oxygen species and increased vasoconstrictor activity. To examine the potential involvement of oxidation-sensitive mechanisms in the pathophysiology of renovascular hypertension, blood samples were collected and renal blood flow measured with electron-beam computed tomography in pigs 5 and 10 weeks after induction of unilateral renal artery stenosis (n=7) or sham operation (n=7). Five weeks after procedure, plasma renin activity and mean arterial pressure were elevated in hypertensive pigs. Levels of prostaglandin F2α (PGF2α)–isoprostanes, vasoconstrictors and markers of oxidative stress, also were significantly increased (157±21 versus 99±16 pg/mL;P <0.05) and correlated with both plasma renin activity (r =0.83) and arterial pressure (r =0.82). By 10 weeks, plasma renin activity returned to baseline but arterial pressure remained elevated (144±10 versus 115±5 mm Hg;P <0.05). Isoprostane levels remained high and still correlated directly with the increase in arterial pressure (r =0.7) but not with plasma renin activity. Stenotic kidney blood flow was decreased at both studies. In shock-frozen cortical tissue, ex vivo endogenous intracellular radical scavengers were significantly decreased in both kidneys. The present study demonstrates, for the first time, that in early renovascular hypertension, an increase in plasma renin activity and arterial pressure is associated with increased systemic oxidative stress. When plasma renin activity later declines, PGF2α-isoprostanes remain elevated, possibly due to local activation or slow responses to angiotensin II, and may participate in sustenance of arterial pressure. Moreover, oxidation-sensitive mechanisms may influence ischemic and hypertensive parenchymal renal injury.</description><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>Dinoprost - analogs & derivatives</subject><subject>Dinoprost - blood</subject><subject>Experimental diseases</subject><subject>F2-Isoprostanes</subject><subject>Female</subject><subject>Free Radical Scavengers - analysis</subject><subject>Hypertension, Renovascular - blood</subject><subject>Hypertension, Renovascular - etiology</subject><subject>Hypertension, Renovascular - physiopathology</subject><subject>Kidney Cortex - blood supply</subject><subject>Kidney Cortex - metabolism</subject><subject>Medical sciences</subject><subject>Oxidative Stress</subject><subject>Renal Artery Obstruction - complications</subject><subject>Renal Circulation</subject><subject>Renin - blood</subject><subject>Swine</subject><subject>Thiobarbituric Acid Reactive Substances - analysis</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkN9rFDEQx4Mo9qw--yaLBd92m8nPzaPU1isUWqqCPoVcdpbbmsueyW7b--9NvUPBlwwkn5nM50vIW6ANgIJTCs16t224blgjBTwjC5BM1EIq_pwsKBhRG4DvR-RVzneUghBCvyRHAIxTztmCfLqMPqHL2FXXj0PnpuEeqy9TwpyrIVbnj1tMwwbj5EJ1i3G8d9nPwaVquSsvE8Y8jPE1edG7kPHNoR6TbxfnX8-W9dX158uzj1e1L7vpupUrLyV62Xlj_KrnDhXoTigtWS-oBnRGG4NipbqWdoZiq6RiTmCLVKPmx-TDfu42jb9mzJPdDNljCC7iOGerlWlpsSzg-__Au3FOsexmGZUcQLaiQKd7yKcx54S93RZVl3YWqH1K11Kwyx83lmvLbDEoHe8OY-fVBrt__CHOApwcgBKTC31y0Q_5L2ckhT8fiz31MIYJU_4Z5gdMdo0uTGtbBKhgqq1ZMaFPR11uuOa_AafEkQw</recordid><startdate>200102</startdate><enddate>200102</enddate><creator>Lerman, Lilach O</creator><creator>Nath, Karl A</creator><creator>Rodriguez-Porcel, Martin</creator><creator>Krier, James D</creator><creator>Schwartz, Robert S</creator><creator>Napoli, Claudio</creator><creator>Romero, J Carlos</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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200102</creationdate><title>Increased Oxidative Stress in Experimental Renovascular Hypertension</title><author>Lerman, Lilach O ; Nath, Karl A ; Rodriguez-Porcel, Martin ; Krier, James D ; Schwartz, Robert S ; Napoli, Claudio ; Romero, J Carlos</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5417-85bc55ec5dc99cbf3ae617d46752f4071ea9799e4b6d80d90e86562a4e8e07e73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><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>Dinoprost - analogs & derivatives</topic><topic>Dinoprost - blood</topic><topic>Experimental diseases</topic><topic>F2-Isoprostanes</topic><topic>Female</topic><topic>Free Radical Scavengers - analysis</topic><topic>Hypertension, Renovascular - blood</topic><topic>Hypertension, Renovascular - etiology</topic><topic>Hypertension, Renovascular - physiopathology</topic><topic>Kidney Cortex - blood supply</topic><topic>Kidney Cortex - metabolism</topic><topic>Medical sciences</topic><topic>Oxidative Stress</topic><topic>Renal Artery Obstruction - complications</topic><topic>Renal Circulation</topic><topic>Renin - blood</topic><topic>Swine</topic><topic>Thiobarbituric Acid Reactive Substances - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lerman, Lilach O</creatorcontrib><creatorcontrib>Nath, Karl A</creatorcontrib><creatorcontrib>Rodriguez-Porcel, Martin</creatorcontrib><creatorcontrib>Krier, James D</creatorcontrib><creatorcontrib>Schwartz, Robert S</creatorcontrib><creatorcontrib>Napoli, Claudio</creatorcontrib><creatorcontrib>Romero, J Carlos</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 Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lerman, Lilach O</au><au>Nath, Karl A</au><au>Rodriguez-Porcel, Martin</au><au>Krier, James D</au><au>Schwartz, Robert S</au><au>Napoli, Claudio</au><au>Romero, J Carlos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased Oxidative Stress in Experimental Renovascular Hypertension</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2001-02</date><risdate>2001</risdate><volume>37</volume><issue>2, Part 2 Suppl</issue><spage>541</spage><epage>546</epage><pages>541-546</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>The pathophysiological mechanisms responsible for maintenance of chronic renovascular hypertension remain undefined. Excess angiotensin II generation may lead to release of reactive oxygen species and increased vasoconstrictor activity. To examine the potential involvement of oxidation-sensitive mechanisms in the pathophysiology of renovascular hypertension, blood samples were collected and renal blood flow measured with electron-beam computed tomography in pigs 5 and 10 weeks after induction of unilateral renal artery stenosis (n=7) or sham operation (n=7). Five weeks after procedure, plasma renin activity and mean arterial pressure were elevated in hypertensive pigs. Levels of prostaglandin F2α (PGF2α)–isoprostanes, vasoconstrictors and markers of oxidative stress, also were significantly increased (157±21 versus 99±16 pg/mL;P <0.05) and correlated with both plasma renin activity (r =0.83) and arterial pressure (r =0.82). By 10 weeks, plasma renin activity returned to baseline but arterial pressure remained elevated (144±10 versus 115±5 mm Hg;P <0.05). Isoprostane levels remained high and still correlated directly with the increase in arterial pressure (r =0.7) but not with plasma renin activity. Stenotic kidney blood flow was decreased at both studies. In shock-frozen cortical tissue, ex vivo endogenous intracellular radical scavengers were significantly decreased in both kidneys. The present study demonstrates, for the first time, that in early renovascular hypertension, an increase in plasma renin activity and arterial pressure is associated with increased systemic oxidative stress. When plasma renin activity later declines, PGF2α-isoprostanes remain elevated, possibly due to local activation or slow responses to angiotensin II, and may participate in sustenance of arterial pressure. Moreover, oxidation-sensitive mechanisms may influence ischemic and hypertensive parenchymal renal injury.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>11230332</pmid><doi>10.1161/01.hyp.37.2.541</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 2001-02, Vol.37 (2, Part 2 Suppl), p.541-546 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure Cardiology. Vascular system Dinoprost - analogs & derivatives Dinoprost - blood Experimental diseases F2-Isoprostanes Female Free Radical Scavengers - analysis Hypertension, Renovascular - blood Hypertension, Renovascular - etiology Hypertension, Renovascular - physiopathology Kidney Cortex - blood supply Kidney Cortex - metabolism Medical sciences Oxidative Stress Renal Artery Obstruction - complications Renal Circulation Renin - blood Swine Thiobarbituric Acid Reactive Substances - analysis |
| title | Increased Oxidative Stress in Experimental Renovascular Hypertension |
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