Normalization of Blood Pressure and Renal Vascular Resistance in SHR With a Membrane-Permeable Superoxide Dismutase Mimetic: Role of Nitric Oxide
Superoxide radical (O2) is increased in the vessel wall of spontaneously hypertensive rats (SHR) where its blockade potentiates endothelium-dependent vasodilation. The purpose of this study was to determine the role of O2 in the hypertension and renal vasoconstriction of SHR and its interaction with...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 1998-07, Vol.32 (1), p.59-64 |
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| creator | Schnackenberg, Christine G Welch, William J Wilcox, Christopher S |
| description | Superoxide radical (O2) is increased in the vessel wall of spontaneously hypertensive rats (SHR) where its blockade potentiates endothelium-dependent vasodilation. The purpose of this study was to determine the role of O2 in the hypertension and renal vasoconstriction of SHR and its interaction with nitric oxide (NO). Baseline mean arterial pressure (MAP) and renal vascular resistance were markedly elevated in SHR (n=6) compared with Wistar-Kyoto rats (WKY; n=6) (145 +/- 4 versus 118 +/- 4 mm Hg, P |
| doi_str_mv | 10.1161/01.HYP.32.1.59 |
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The purpose of this study was to determine the role of O2 in the hypertension and renal vasoconstriction of SHR and its interaction with nitric oxide (NO). Baseline mean arterial pressure (MAP) and renal vascular resistance were markedly elevated in SHR (n=6) compared with Wistar-Kyoto rats (WKY; n=6) (145 +/- 4 versus 118 +/- 4 mm Hg, P<0.05, and 24 +/- 3 versus 17 +/- 1 mm Hg [middle dot] mL [middle dot] min, respectively; P<0.05). The stable membrane-permeable superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl (tempol; 72 [micro sign]mol/kg IV) normalized MAP (103 +/- 9 versus 96 +/- 6 mm Hg for SHR and WKY, respectively) and RVR (17 +/- 2 versus 15 +/- 1 mm Hg [middle dot] mL [middle dot] min) of SHR. The MAP of SHR was more sensitive and responsive to graded infusions of tempol (0, 1.8, 18, 180, and 1800 [micro sign]mol [middle dot] kg [middle dot] h IV) than that of WKY. To determine whether O (2) increases MAP by inactivation of NO, its synthesis was blocked in SHR with N methyl ester (L-NAME, 11 [micro sign]mol [middle dot] kg [middle dot] min IV, n=6). Whereas tempol alone significantly reduced MAP by 32% (184 +/- 12 to 121 +/- 18 mm Hg, P<0.05, n=6), L-NAME infusion abolished the MAP response to tempol (187 +/- 8 to 186 +/- 4 mm Hg, n=5). In contrast, tempol did reduce MAP of SHR (188 +/- 7 to 161 +/- 7 mm Hg, P<0.05) where MAP was elevated by norepinephrine (31 nmol [middle dot] kg [middle dot] min IV, n=6). Finally, to determine the longer-term effect of O2, tempol (1.5 mmol [middle dot] kg [middle dot] d IP) was given for 7 days. Tempol had no effect on MAP in WKY (96 +/- 1 to 97 +/- 1 mm Hg, n=7) but significantly decreased MAP in SHR (133 +/- 2 to 120 +/- 3 mm Hg, P<0.05, n=7). These data implicate O2 in the hypertension of SHR in vivo. The antihypertensive action of tempol depends on NO synthesis presumably because O2 inactivates NO and thus diminishes its vasodilatory actions. (Hypertension. 1998;32:59-64.)</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.32.1.59</identifier><identifier>PMID: 9674638</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Antioxidants - administration & dosage ; Antioxidants - pharmacology ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Cyclic N-Oxides - administration & dosage ; Cyclic N-Oxides - pharmacology ; Free Radical Scavengers - administration & dosage ; Free Radical Scavengers - pharmacology ; Free Radicals ; Kidney - drug effects ; Male ; Medical sciences ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - antagonists & inhibitors ; Nitric Oxide - biosynthesis ; Nitric Oxide - physiology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Renal Circulation - drug effects ; Spin Labels ; Superoxide Dismutase - physiology ; Superoxides - metabolism ; Time Factors ; Vascular Resistance - drug effects</subject><ispartof>Hypertension (Dallas, Tex. 1979), 1998-07, Vol.32 (1), p.59-64</ispartof><rights>1998 American Heart Association, Inc.</rights><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jul 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3860-8c98d7d78be2087d8a467511773c698a6a0a5fea1e78bc10229b4c99367fc5473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,3687,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2337692$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9674638$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schnackenberg, Christine G</creatorcontrib><creatorcontrib>Welch, William J</creatorcontrib><creatorcontrib>Wilcox, Christopher S</creatorcontrib><title>Normalization of Blood Pressure and Renal Vascular Resistance in SHR With a Membrane-Permeable Superoxide Dismutase Mimetic: Role of Nitric Oxide</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Superoxide radical (O2) is increased in the vessel wall of spontaneously hypertensive rats (SHR) where its blockade potentiates endothelium-dependent vasodilation. The purpose of this study was to determine the role of O2 in the hypertension and renal vasoconstriction of SHR and its interaction with nitric oxide (NO). Baseline mean arterial pressure (MAP) and renal vascular resistance were markedly elevated in SHR (n=6) compared with Wistar-Kyoto rats (WKY; n=6) (145 +/- 4 versus 118 +/- 4 mm Hg, P<0.05, and 24 +/- 3 versus 17 +/- 1 mm Hg [middle dot] mL [middle dot] min, respectively; P<0.05). The stable membrane-permeable superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl (tempol; 72 [micro sign]mol/kg IV) normalized MAP (103 +/- 9 versus 96 +/- 6 mm Hg for SHR and WKY, respectively) and RVR (17 +/- 2 versus 15 +/- 1 mm Hg [middle dot] mL [middle dot] min) of SHR. The MAP of SHR was more sensitive and responsive to graded infusions of tempol (0, 1.8, 18, 180, and 1800 [micro sign]mol [middle dot] kg [middle dot] h IV) than that of WKY. To determine whether O (2) increases MAP by inactivation of NO, its synthesis was blocked in SHR with N methyl ester (L-NAME, 11 [micro sign]mol [middle dot] kg [middle dot] min IV, n=6). Whereas tempol alone significantly reduced MAP by 32% (184 +/- 12 to 121 +/- 18 mm Hg, P<0.05, n=6), L-NAME infusion abolished the MAP response to tempol (187 +/- 8 to 186 +/- 4 mm Hg, n=5). In contrast, tempol did reduce MAP of SHR (188 +/- 7 to 161 +/- 7 mm Hg, P<0.05) where MAP was elevated by norepinephrine (31 nmol [middle dot] kg [middle dot] min IV, n=6). Finally, to determine the longer-term effect of O2, tempol (1.5 mmol [middle dot] kg [middle dot] d IP) was given for 7 days. Tempol had no effect on MAP in WKY (96 +/- 1 to 97 +/- 1 mm Hg, n=7) but significantly decreased MAP in SHR (133 +/- 2 to 120 +/- 3 mm Hg, P<0.05, n=7). These data implicate O2 in the hypertension of SHR in vivo. The antihypertensive action of tempol depends on NO synthesis presumably because O2 inactivates NO and thus diminishes its vasodilatory actions. (Hypertension. 1998;32:59-64.)</description><subject>Animals</subject><subject>Antioxidants - administration & dosage</subject><subject>Antioxidants - pharmacology</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>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Cyclic N-Oxides - administration & dosage</subject><subject>Cyclic N-Oxides - pharmacology</subject><subject>Free Radical Scavengers - administration & dosage</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Free Radicals</subject><subject>Kidney - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - antagonists & inhibitors</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide - physiology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Renal Circulation - drug effects</subject><subject>Spin Labels</subject><subject>Superoxide Dismutase - physiology</subject><subject>Superoxides - metabolism</subject><subject>Time Factors</subject><subject>Vascular Resistance - drug effects</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkVuLFDEQhRtR1nX11TchiPjWbW6di2-6XkbYyzDr9Slk0tVMdtOdMelm1X_hPzbDDPtgQSiK-jhFzqmqpwQ3hAjyCpNm8WPZMNqQptX3qmPSUl7zVrD71TEmmteakO8Pq0c5X2NMOOfyqDrSQnLB1HH19yKmwQb_x04-jij26G2IsUPLBDnPCZAdO7SC0Qb01WY3B5vKmH2e7OgA-RFdLVbom582yKJzGNbJjlAvIQ1g1wHQ1byFFH_5DtA7n4d5shnQuR9g8u41WsWClJsXfkreocsd97h60NuQ4cmhn1RfPrz_fLqozy4_fjp9c1Y7pgSuldOqk51Ua6BYyU5ZLmRLiJTMCa2ssNi2PVgCBXEEU6rX3GnNhOxdyyU7qV7udbcp_pwhT2bw2UEI5QNxzkYVt7SUuoDP_wOv45yKI9lQ3FIlJGMFavaQSzHnBL3ZJj_Y9NsQbHZBGUxMCcowaohpd6rPDqrzeoDuDj8kU_YvDvtiuw198dX5fIdRxqTQtGB8j93GMEHKN2G-hWQ2YMO0MbgUp0LVRGuFZZnq8ghm_wA5DKqM</recordid><startdate>199807</startdate><enddate>199807</enddate><creator>Schnackenberg, Christine G</creator><creator>Welch, William J</creator><creator>Wilcox, Christopher S</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>199807</creationdate><title>Normalization of Blood Pressure and Renal Vascular Resistance in SHR With a Membrane-Permeable Superoxide Dismutase Mimetic: Role of Nitric Oxide</title><author>Schnackenberg, Christine G ; Welch, William J ; Wilcox, Christopher S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3860-8c98d7d78be2087d8a467511773c698a6a0a5fea1e78bc10229b4c99367fc5473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Antioxidants - administration & dosage</topic><topic>Antioxidants - pharmacology</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>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Cyclic N-Oxides - administration & dosage</topic><topic>Cyclic N-Oxides - pharmacology</topic><topic>Free Radical Scavengers - administration & dosage</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Free Radicals</topic><topic>Kidney - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - antagonists & inhibitors</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide - physiology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Renal Circulation - drug effects</topic><topic>Spin Labels</topic><topic>Superoxide Dismutase - physiology</topic><topic>Superoxides - metabolism</topic><topic>Time Factors</topic><topic>Vascular Resistance - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schnackenberg, Christine G</creatorcontrib><creatorcontrib>Welch, William J</creatorcontrib><creatorcontrib>Wilcox, Christopher 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 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>Schnackenberg, Christine G</au><au>Welch, William J</au><au>Wilcox, Christopher S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Normalization of Blood Pressure and Renal Vascular Resistance in SHR With a Membrane-Permeable Superoxide Dismutase Mimetic: Role of Nitric Oxide</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1998-07</date><risdate>1998</risdate><volume>32</volume><issue>1</issue><spage>59</spage><epage>64</epage><pages>59-64</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Superoxide radical (O2) is increased in the vessel wall of spontaneously hypertensive rats (SHR) where its blockade potentiates endothelium-dependent vasodilation. The purpose of this study was to determine the role of O2 in the hypertension and renal vasoconstriction of SHR and its interaction with nitric oxide (NO). Baseline mean arterial pressure (MAP) and renal vascular resistance were markedly elevated in SHR (n=6) compared with Wistar-Kyoto rats (WKY; n=6) (145 +/- 4 versus 118 +/- 4 mm Hg, P<0.05, and 24 +/- 3 versus 17 +/- 1 mm Hg [middle dot] mL [middle dot] min, respectively; P<0.05). The stable membrane-permeable superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl (tempol; 72 [micro sign]mol/kg IV) normalized MAP (103 +/- 9 versus 96 +/- 6 mm Hg for SHR and WKY, respectively) and RVR (17 +/- 2 versus 15 +/- 1 mm Hg [middle dot] mL [middle dot] min) of SHR. The MAP of SHR was more sensitive and responsive to graded infusions of tempol (0, 1.8, 18, 180, and 1800 [micro sign]mol [middle dot] kg [middle dot] h IV) than that of WKY. To determine whether O (2) increases MAP by inactivation of NO, its synthesis was blocked in SHR with N methyl ester (L-NAME, 11 [micro sign]mol [middle dot] kg [middle dot] min IV, n=6). Whereas tempol alone significantly reduced MAP by 32% (184 +/- 12 to 121 +/- 18 mm Hg, P<0.05, n=6), L-NAME infusion abolished the MAP response to tempol (187 +/- 8 to 186 +/- 4 mm Hg, n=5). In contrast, tempol did reduce MAP of SHR (188 +/- 7 to 161 +/- 7 mm Hg, P<0.05) where MAP was elevated by norepinephrine (31 nmol [middle dot] kg [middle dot] min IV, n=6). Finally, to determine the longer-term effect of O2, tempol (1.5 mmol [middle dot] kg [middle dot] d IP) was given for 7 days. Tempol had no effect on MAP in WKY (96 +/- 1 to 97 +/- 1 mm Hg, n=7) but significantly decreased MAP in SHR (133 +/- 2 to 120 +/- 3 mm Hg, P<0.05, n=7). These data implicate O2 in the hypertension of SHR in vivo. The antihypertensive action of tempol depends on NO synthesis presumably because O2 inactivates NO and thus diminishes its vasodilatory actions. (Hypertension. 1998;32:59-64.)</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9674638</pmid><doi>10.1161/01.HYP.32.1.59</doi><tpages>6</tpages></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 1998-07, Vol.32 (1), p.59-64 |
| issn | 0194-911X 1524-4563 |
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| subjects | Animals Antioxidants - administration & dosage Antioxidants - pharmacology Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure - drug effects Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Cyclic N-Oxides - administration & dosage Cyclic N-Oxides - pharmacology Free Radical Scavengers - administration & dosage Free Radical Scavengers - pharmacology Free Radicals Kidney - drug effects Male Medical sciences NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - antagonists & inhibitors Nitric Oxide - biosynthesis Nitric Oxide - physiology Rats Rats, Inbred SHR Rats, Inbred WKY Renal Circulation - drug effects Spin Labels Superoxide Dismutase - physiology Superoxides - metabolism Time Factors Vascular Resistance - drug effects |
| title | Normalization of Blood Pressure and Renal Vascular Resistance in SHR With a Membrane-Permeable Superoxide Dismutase Mimetic: Role of Nitric Oxide |
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