Mechanisms of salt-sensitive hypertension: role of renal medullary inducible nitric oxide synthase
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216 The goal of this study was to determine the role of renal medullary inducible nitric oxide synthase (iNOS) in the arterial pressure, renal hemodynamic, and renal excretory changes that occur...
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| Veröffentlicht in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2003-02, Vol.284 (2), p.372-R379 |
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| container_issue | 2 |
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| container_title | American journal of physiology. Regulatory, integrative and comparative physiology |
| container_volume | 284 |
| creator | Tian, Niu Gannon, Anthony W Khalil, Raouf A Manning, R. Davis, Jr |
| description | Department of Physiology and Biophysics, University of
Mississippi Medical Center, Jackson, Mississippi 39216
The goal of this study was to
determine the role of renal medullary inducible nitric oxide synthase
(iNOS) in the arterial pressure, renal hemodynamic, and renal excretory
changes that occur in Dahl/Rapp salt-resistant (R) and salt-sensitive
(S) rats during high Na intake. Forty R and S rats, equipped with
indwelling arterial, venous, and renal medullary catheters, were
subjected to high (8%) Na intake, and selective iNOS inhibition was
achieved with continuous intravenous or renal medullary
interstitial infusion of aminoguanidine (AG; 3.075 mg · kg 1 · h 1 ). After 5 days of AG, mean arterial pressure increased to 132 ± 2%
control in the S rats with high Na intake and intramedullary AG
compared with 121 ± 4% control ( P |
| doi_str_mv | 10.1152/ajpregu.00509.2002 |
| format | Article |
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Mississippi Medical Center, Jackson, Mississippi 39216
The goal of this study was to
determine the role of renal medullary inducible nitric oxide synthase
(iNOS) in the arterial pressure, renal hemodynamic, and renal excretory
changes that occur in Dahl/Rapp salt-resistant (R) and salt-sensitive
(S) rats during high Na intake. Forty R and S rats, equipped with
indwelling arterial, venous, and renal medullary catheters, were
subjected to high (8%) Na intake, and selective iNOS inhibition was
achieved with continuous intravenous or renal medullary
interstitial infusion of aminoguanidine (AG; 3.075 mg · kg 1 · h 1 ). After 5 days of AG, mean arterial pressure increased to 132 ± 2%
control in the S rats with high Na intake and intramedullary AG
compared with 121 ± 4% control ( P < 0.05) in
the S rats with high Na intake alone and 121 ± 2% control
( P < 0.05) in the S rats with high Na intake and
intravenous AG. AG did not change arterial pressure in R rats. AG also
caused little change in renal hemodynamics, urinary Na, or
H 2 O excretion or ACh-induced aortic vasorelaxation in R or
S rats. The data suggest that during high Na intake, nitric oxide
produced by renal medullary iNOS helps to prevent excessive increases
in arterial pressure in the Dahl S rat but not the R rat.
renal hemodynamics; endothelial function</description><identifier>ISSN: 0363-6119</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.00509.2002</identifier><identifier>PMID: 12399250</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Aorta - drug effects ; Aorta - physiology ; Blood Pressure - drug effects ; Enzyme Induction - drug effects ; Glomerular Filtration Rate - drug effects ; Guanidines - pharmacology ; Heart Rate - drug effects ; Hypertension - enzymology ; Hypertension - physiopathology ; Kidney Medulla - blood supply ; Kidney Medulla - drug effects ; Kidney Medulla - enzymology ; Kidney Medulla - physiopathology ; Male ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Rats ; Rats, Inbred Dahl ; Renal Circulation - drug effects ; Sodium - administration & dosage ; Sodium - pharmacology ; Sodium - urine ; Time Factors ; Vasodilation - drug effects</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 2003-02, Vol.284 (2), p.372-R379</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-ed531f1c08e0b4f206277a370a4c694b91de2333a3039bf6609744480c076cc63</citedby><cites>FETCH-LOGICAL-c453t-ed531f1c08e0b4f206277a370a4c694b91de2333a3039bf6609744480c076cc63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3025,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12399250$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tian, Niu</creatorcontrib><creatorcontrib>Gannon, Anthony W</creatorcontrib><creatorcontrib>Khalil, Raouf A</creatorcontrib><creatorcontrib>Manning, R. Davis, Jr</creatorcontrib><title>Mechanisms of salt-sensitive hypertension: role of renal medullary inducible nitric oxide synthase</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>Department of Physiology and Biophysics, University of
Mississippi Medical Center, Jackson, Mississippi 39216
The goal of this study was to
determine the role of renal medullary inducible nitric oxide synthase
(iNOS) in the arterial pressure, renal hemodynamic, and renal excretory
changes that occur in Dahl/Rapp salt-resistant (R) and salt-sensitive
(S) rats during high Na intake. Forty R and S rats, equipped with
indwelling arterial, venous, and renal medullary catheters, were
subjected to high (8%) Na intake, and selective iNOS inhibition was
achieved with continuous intravenous or renal medullary
interstitial infusion of aminoguanidine (AG; 3.075 mg · kg 1 · h 1 ). After 5 days of AG, mean arterial pressure increased to 132 ± 2%
control in the S rats with high Na intake and intramedullary AG
compared with 121 ± 4% control ( P < 0.05) in
the S rats with high Na intake alone and 121 ± 2% control
( P < 0.05) in the S rats with high Na intake and
intravenous AG. AG did not change arterial pressure in R rats. AG also
caused little change in renal hemodynamics, urinary Na, or
H 2 O excretion or ACh-induced aortic vasorelaxation in R or
S rats. The data suggest that during high Na intake, nitric oxide
produced by renal medullary iNOS helps to prevent excessive increases
in arterial pressure in the Dahl S rat but not the R rat.
renal hemodynamics; endothelial function</description><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Aorta - physiology</subject><subject>Blood Pressure - drug effects</subject><subject>Enzyme Induction - drug effects</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Guanidines - pharmacology</subject><subject>Heart Rate - drug effects</subject><subject>Hypertension - enzymology</subject><subject>Hypertension - physiopathology</subject><subject>Kidney Medulla - blood supply</subject><subject>Kidney Medulla - drug effects</subject><subject>Kidney Medulla - enzymology</subject><subject>Kidney Medulla - physiopathology</subject><subject>Male</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Rats</subject><subject>Rats, Inbred Dahl</subject><subject>Renal Circulation - drug effects</subject><subject>Sodium - administration & dosage</subject><subject>Sodium - pharmacology</subject><subject>Sodium - urine</subject><subject>Time Factors</subject><subject>Vasodilation - drug effects</subject><issn>0363-6119</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtu2zAQRYkiQeO4_YEuAq2ykzt8SDS7K4wmKZAiQOCsCYoaWTRkSSGlNPr7UrHbrLoiBnPuBecQ8oXCitKMfTX73uNuXAFkoFYMgH0gi7hgKRUKzsgCeM7TnFJ1QS5D2AOA4IJ_JBeUcaVYBgtS_EJbm9aFQ0i6KgmmGdKAbXCDe8Gknnr0wzx27bfEdw3OkMfWNMkBy7FpjJ8S15ajdUVctm7wzibdqysxCVM71CbgJ3JemSbg59O7JE83P7abu_T-4fbn5vt9akXGhxTLjNOKWlgjFKJikDMpDZdghM2VKBQtkXHODQeuiirPQUkhxBosyNzanC_J9bG3993ziGHQBxcsxj-22I1BS6YyKaSIIDuC1ncheKx0790hXqIp6NmsPpnVb2b1bDaGrk7tYxFPf4-cVEYgPQK129W_nUfd11MU13S76V8hWwvN9COXc6H6P38T1W7xdfgbfM_pvqz4HwwgnGE</recordid><startdate>20030201</startdate><enddate>20030201</enddate><creator>Tian, Niu</creator><creator>Gannon, Anthony W</creator><creator>Khalil, Raouf A</creator><creator>Manning, R. Davis, Jr</creator><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>20030201</creationdate><title>Mechanisms of salt-sensitive hypertension: role of renal medullary inducible nitric oxide synthase</title><author>Tian, Niu ; Gannon, Anthony W ; Khalil, Raouf A ; Manning, R. Davis, Jr</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-ed531f1c08e0b4f206277a370a4c694b91de2333a3039bf6609744480c076cc63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Aorta - drug effects</topic><topic>Aorta - physiology</topic><topic>Blood Pressure - drug effects</topic><topic>Enzyme Induction - drug effects</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Guanidines - pharmacology</topic><topic>Heart Rate - drug effects</topic><topic>Hypertension - enzymology</topic><topic>Hypertension - physiopathology</topic><topic>Kidney Medulla - blood supply</topic><topic>Kidney Medulla - drug effects</topic><topic>Kidney Medulla - enzymology</topic><topic>Kidney Medulla - physiopathology</topic><topic>Male</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Rats</topic><topic>Rats, Inbred Dahl</topic><topic>Renal Circulation - drug effects</topic><topic>Sodium - administration & dosage</topic><topic>Sodium - pharmacology</topic><topic>Sodium - urine</topic><topic>Time Factors</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tian, Niu</creatorcontrib><creatorcontrib>Gannon, Anthony W</creatorcontrib><creatorcontrib>Khalil, Raouf A</creatorcontrib><creatorcontrib>Manning, R. Davis, Jr</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tian, Niu</au><au>Gannon, Anthony W</au><au>Khalil, Raouf A</au><au>Manning, R. Davis, Jr</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of salt-sensitive hypertension: role of renal medullary inducible nitric oxide synthase</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2003-02-01</date><risdate>2003</risdate><volume>284</volume><issue>2</issue><spage>372</spage><epage>R379</epage><pages>372-R379</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><abstract>Department of Physiology and Biophysics, University of
Mississippi Medical Center, Jackson, Mississippi 39216
The goal of this study was to
determine the role of renal medullary inducible nitric oxide synthase
(iNOS) in the arterial pressure, renal hemodynamic, and renal excretory
changes that occur in Dahl/Rapp salt-resistant (R) and salt-sensitive
(S) rats during high Na intake. Forty R and S rats, equipped with
indwelling arterial, venous, and renal medullary catheters, were
subjected to high (8%) Na intake, and selective iNOS inhibition was
achieved with continuous intravenous or renal medullary
interstitial infusion of aminoguanidine (AG; 3.075 mg · kg 1 · h 1 ). After 5 days of AG, mean arterial pressure increased to 132 ± 2%
control in the S rats with high Na intake and intramedullary AG
compared with 121 ± 4% control ( P < 0.05) in
the S rats with high Na intake alone and 121 ± 2% control
( P < 0.05) in the S rats with high Na intake and
intravenous AG. AG did not change arterial pressure in R rats. AG also
caused little change in renal hemodynamics, urinary Na, or
H 2 O excretion or ACh-induced aortic vasorelaxation in R or
S rats. The data suggest that during high Na intake, nitric oxide
produced by renal medullary iNOS helps to prevent excessive increases
in arterial pressure in the Dahl S rat but not the R rat.
renal hemodynamics; endothelial function</abstract><cop>United States</cop><pmid>12399250</pmid><doi>10.1152/ajpregu.00509.2002</doi></addata></record> |
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| identifier | ISSN: 0363-6119 |
| ispartof | American journal of physiology. Regulatory, integrative and comparative physiology, 2003-02, Vol.284 (2), p.372-R379 |
| issn | 0363-6119 1522-1490 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpregu_284_2_R372 |
| source | MEDLINE; American Physiological Society Paid; EZB Electronic Journals Library |
| subjects | Animals Aorta - drug effects Aorta - physiology Blood Pressure - drug effects Enzyme Induction - drug effects Glomerular Filtration Rate - drug effects Guanidines - pharmacology Heart Rate - drug effects Hypertension - enzymology Hypertension - physiopathology Kidney Medulla - blood supply Kidney Medulla - drug effects Kidney Medulla - enzymology Kidney Medulla - physiopathology Male Nitric Oxide - metabolism Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Rats Rats, Inbred Dahl Renal Circulation - drug effects Sodium - administration & dosage Sodium - pharmacology Sodium - urine Time Factors Vasodilation - drug effects |
| title | Mechanisms of salt-sensitive hypertension: role of renal medullary inducible nitric oxide synthase |
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