Salt-sensitive hypertension in conscious rats induced by chronic nitric oxide blockade
This study examined the effects of alterations in salt-intake on blood pressure (BP) in rats chronically treated intravenously with or without the nitric oxide synthase (NOS) inhibitor N G-nitro- l-arginine methyl ester (L-NAME) (8.6 mg/kg/day). The changes in mean arterial pressure (MAP), the renal...
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| Veröffentlicht in: | American journal of hypertension 2002-02, Vol.15 (2), p.150-156 |
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| creator | Nakanishi, Kazushige Hara, Noriko Nagai, Yohko |
| description | This study examined the effects of alterations in salt-intake on blood pressure (BP) in rats chronically treated intravenously with or without the nitric oxide synthase (NOS) inhibitor N
G-nitro-
l-arginine methyl ester (L-NAME) (8.6 mg/kg/day). The changes in mean arterial pressure (MAP), the renal cortical and medullary blood flow (CBF and MBF), and the sodium balance were determined by implanted optical fibers and laser-Doppler flow measurement techniques in the conscious rats. The results showed that high salt intake (7.4 mEq/day) elevates CBF (139% ± 15%), but has no significant effect on MAP or MBF in control rats; in L-NAME-treated rats, high salt intake elevates MAP, produces no change in CBF, and decreases MBF (51% ± 14%), as well as increasing the sodium balance (0.26 ± 0.23 mEq/day to 1.29 ± 0.47 mEq/day).
The present experiments indicated that NO appears to maintain the MBF during high salt intake and to prevent the changes in MAP, and, in the absence of NO, salt-sensitive hypertension develops. Nitric oxide plays an important role in the development of salt-sensitive hypertension with the change of MBF. |
| doi_str_mv | 10.1016/S0895-7061(01)02267-1 |
| format | Article |
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G-nitro-
l-arginine methyl ester (L-NAME) (8.6 mg/kg/day). The changes in mean arterial pressure (MAP), the renal cortical and medullary blood flow (CBF and MBF), and the sodium balance were determined by implanted optical fibers and laser-Doppler flow measurement techniques in the conscious rats. The results showed that high salt intake (7.4 mEq/day) elevates CBF (139% ± 15%), but has no significant effect on MAP or MBF in control rats; in L-NAME-treated rats, high salt intake elevates MAP, produces no change in CBF, and decreases MBF (51% ± 14%), as well as increasing the sodium balance (0.26 ± 0.23 mEq/day to 1.29 ± 0.47 mEq/day).
The present experiments indicated that NO appears to maintain the MBF during high salt intake and to prevent the changes in MAP, and, in the absence of NO, salt-sensitive hypertension develops. Nitric oxide plays an important role in the development of salt-sensitive hypertension with the change of MBF.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/S0895-7061(01)02267-1</identifier><identifier>PMID: 11863250</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Cardiology. Vascular system ; Dose-Response Relationship, Drug ; Enzyme Inhibitors ; Experimental diseases ; Hypertension - chemically induced ; Hypertension - physiopathology ; Kidney Cortex - blood supply ; Kidney Medulla - blood supply ; Male ; Medical sciences ; medullary blood flow ; NG-Nitroarginine Methyl Ester ; nitric oxide ; Nitric Oxide - antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Renal Circulation - drug effects ; Salt-sensitive hypertension ; Sodium - metabolism ; Sodium Chloride - administration & dosage ; Sodium Chloride - pharmacology</subject><ispartof>American journal of hypertension, 2002-02, Vol.15 (2), p.150-156</ispartof><rights>2002 American Journal of Hypertension, Ltd.</rights><rights>American Journal of Hypertension, Ltd. © 2002 by the American Journal of Hypertension, Ltd. 2002</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c569t-6ce5300388952c6dd1c358c5492e6ba8bb9e1a9321733e221d35c8c7c5a414403</citedby><cites>FETCH-LOGICAL-c569t-6ce5300388952c6dd1c358c5492e6ba8bb9e1a9321733e221d35c8c7c5a414403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13496382$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11863250$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakanishi, Kazushige</creatorcontrib><creatorcontrib>Hara, Noriko</creatorcontrib><creatorcontrib>Nagai, Yohko</creatorcontrib><title>Salt-sensitive hypertension in conscious rats induced by chronic nitric oxide blockade</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>This study examined the effects of alterations in salt-intake on blood pressure (BP) in rats chronically treated intravenously with or without the nitric oxide synthase (NOS) inhibitor N
G-nitro-
l-arginine methyl ester (L-NAME) (8.6 mg/kg/day). The changes in mean arterial pressure (MAP), the renal cortical and medullary blood flow (CBF and MBF), and the sodium balance were determined by implanted optical fibers and laser-Doppler flow measurement techniques in the conscious rats. The results showed that high salt intake (7.4 mEq/day) elevates CBF (139% ± 15%), but has no significant effect on MAP or MBF in control rats; in L-NAME-treated rats, high salt intake elevates MAP, produces no change in CBF, and decreases MBF (51% ± 14%), as well as increasing the sodium balance (0.26 ± 0.23 mEq/day to 1.29 ± 0.47 mEq/day).
The present experiments indicated that NO appears to maintain the MBF during high salt intake and to prevent the changes in MAP, and, in the absence of NO, salt-sensitive hypertension develops. Nitric oxide plays an important role in the development of salt-sensitive hypertension with the change of MBF.</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 - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Inhibitors</subject><subject>Experimental diseases</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - physiopathology</subject><subject>Kidney Cortex - blood supply</subject><subject>Kidney Medulla - blood supply</subject><subject>Male</subject><subject>Medical sciences</subject><subject>medullary blood flow</subject><subject>NG-Nitroarginine Methyl Ester</subject><subject>nitric oxide</subject><subject>Nitric Oxide - antagonists & inhibitors</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reference Values</subject><subject>Renal Circulation - drug effects</subject><subject>Salt-sensitive hypertension</subject><subject>Sodium - metabolism</subject><subject>Sodium Chloride - administration & dosage</subject><subject>Sodium Chloride - pharmacology</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkW1rFDEUhYNY7Lb6E9QBEfRDNC-TTOZTkdLalopCfcMvIZO5y2a7TdYkU7r_3oyzdCkIQuCS8Jx7wjkIPafkHSVUvr8iqhW4IZK-IfQtYUw2mD5CM6qaFtOWiMdodo_so4OUloSQWkr6BO1TqiRngszQ9yuzyjiBTy67W6gWmzXEPF6Dr5yvbPDJujCkKpqcyks_WOirblPZRQze2cq7HMsId66HqlsFe216eIr25maV4Nl2HqJvpydfj8_w5eeP58cfLrEVss1YWhCcEK7KR5mVfU8tF8qKumUgO6O6rgVqWs5owzkwRnsurLKNFaamdU34IXo17V3H8HuAlPUyDNEXS00Jk6LhtVSFEhNlY0gpwlyvo7sxcVMgPaap_6apx6g0KWdMU9Oie7HdPnQ30O9U2_gK8HoLmGTNah6Nty7tOF63kitWODJxYVj_2xs_8Maj98tJ4k0eItyrzHLBSIGaQuCJcCnD3Q6I11o2vBH67OcvfXrx45OSX7jmhT-aeCiF3DqIujQLvtTpItis--D-k8cfIFS35g</recordid><startdate>20020201</startdate><enddate>20020201</enddate><creator>Nakanishi, Kazushige</creator><creator>Hara, Noriko</creator><creator>Nagai, Yohko</creator><general>Elsevier Inc</general><general>Oxford University Press</general><general>Elsevier Science</general><scope>BSCLL</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20020201</creationdate><title>Salt-sensitive hypertension in conscious rats induced by chronic nitric oxide blockade</title><author>Nakanishi, Kazushige ; Hara, Noriko ; Nagai, Yohko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c569t-6ce5300388952c6dd1c358c5492e6ba8bb9e1a9321733e221d35c8c7c5a414403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</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 - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Inhibitors</topic><topic>Experimental diseases</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - physiopathology</topic><topic>Kidney Cortex - blood supply</topic><topic>Kidney Medulla - blood supply</topic><topic>Male</topic><topic>Medical sciences</topic><topic>medullary blood flow</topic><topic>NG-Nitroarginine Methyl Ester</topic><topic>nitric oxide</topic><topic>Nitric Oxide - antagonists & inhibitors</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reference Values</topic><topic>Renal Circulation - drug effects</topic><topic>Salt-sensitive hypertension</topic><topic>Sodium - metabolism</topic><topic>Sodium Chloride - administration & dosage</topic><topic>Sodium Chloride - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakanishi, Kazushige</creatorcontrib><creatorcontrib>Hara, Noriko</creatorcontrib><creatorcontrib>Nagai, Yohko</creatorcontrib><collection>Istex</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakanishi, Kazushige</au><au>Hara, Noriko</au><au>Nagai, Yohko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Salt-sensitive hypertension in conscious rats induced by chronic nitric oxide blockade</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2002-02-01</date><risdate>2002</risdate><volume>15</volume><issue>2</issue><spage>150</spage><epage>156</epage><pages>150-156</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>This study examined the effects of alterations in salt-intake on blood pressure (BP) in rats chronically treated intravenously with or without the nitric oxide synthase (NOS) inhibitor N
G-nitro-
l-arginine methyl ester (L-NAME) (8.6 mg/kg/day). The changes in mean arterial pressure (MAP), the renal cortical and medullary blood flow (CBF and MBF), and the sodium balance were determined by implanted optical fibers and laser-Doppler flow measurement techniques in the conscious rats. The results showed that high salt intake (7.4 mEq/day) elevates CBF (139% ± 15%), but has no significant effect on MAP or MBF in control rats; in L-NAME-treated rats, high salt intake elevates MAP, produces no change in CBF, and decreases MBF (51% ± 14%), as well as increasing the sodium balance (0.26 ± 0.23 mEq/day to 1.29 ± 0.47 mEq/day).
The present experiments indicated that NO appears to maintain the MBF during high salt intake and to prevent the changes in MAP, and, in the absence of NO, salt-sensitive hypertension develops. Nitric oxide plays an important role in the development of salt-sensitive hypertension with the change of MBF.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>11863250</pmid><doi>10.1016/S0895-7061(01)02267-1</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0895-7061 |
| ispartof | American journal of hypertension, 2002-02, Vol.15 (2), p.150-156 |
| issn | 0895-7061 1879-1905 1941-7225 |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure - drug effects Cardiology. Vascular system Dose-Response Relationship, Drug Enzyme Inhibitors Experimental diseases Hypertension - chemically induced Hypertension - physiopathology Kidney Cortex - blood supply Kidney Medulla - blood supply Male Medical sciences medullary blood flow NG-Nitroarginine Methyl Ester nitric oxide Nitric Oxide - antagonists & inhibitors Rats Rats, Sprague-Dawley Reference Values Renal Circulation - drug effects Salt-sensitive hypertension Sodium - metabolism Sodium Chloride - administration & dosage Sodium Chloride - pharmacology |
| title | Salt-sensitive hypertension in conscious rats induced by chronic nitric oxide blockade |
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