Differential nNOS gene expression in salt-sensitive and salt-resistant Dahl rats
BACKGROUNDSeveral indications exist to suggest that an impaired production of nitric oxide might have a role in the development of salt-sensitive hypertension. OBJECTIVETo examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with...
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| Veröffentlicht in: | Journal of hypertension 2001-07, Vol.19 (7), p.1223-1231 |
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| container_title | Journal of hypertension |
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| creator | Castrop, Hayo Kurtz, Armin |
| description | BACKGROUNDSeveral indications exist to suggest that an impaired production of nitric oxide might have a role in the development of salt-sensitive hypertension.
OBJECTIVETo examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with that in the salt-resistant Dahl rat.
DESIGN AND METHODSThe abundance of NOS mRNA was measured by RNase protection assay in different organs of salt-resistant and salt-sensitive Dahl rats. In addition, the zonal expression of NOS genes in the kidney under salt load and salt restriction was determined.
RESULTSThe abundance of endothelial NOS mRNA was similar between the salt-resistant and salt-sensitive Dahl rat strains in all organs. Inducible NOS mRNA was not detectable by RNase protection assay in any organ. Neuronal NOS (nNOS) mRNA expression, however, was about 50% lower in brain and kidney of salt-sensitive Dahl rats than in salt-resistant Dahl rats. Within the kidney, nNOS mRNA levels were significantly decreased in salt-sensitive Dahl rats compared with those in salt-resistant Dahl rats, in cortex, outer and inner medulla (50, 40 and 30%, respectively) under all dietary conditions. A comparison of renal nNOS gene expression in Dahl rats with that in salt-insensitive Sprague–Dawley rats revealed that the abundance of renal nNOS was similar in salt-sensitive Dahl and Sprague–Dawley rats, but was increased in salt-resistant Dahl rats relative to that in Sprague–Dawley rats.
CONCLUSIONThese data suggest that nNOS gene expression is increased in salt-resistant Dahl rats compared with that in salt-sensitive Dahl rats. This increased nNOS expression of the salt-resistant Dahl strain might play a part in compensating for a defect of renal salt excretion in the Dahl strains. |
| doi_str_mv | 10.1097/00004872-200107000-00007 |
| format | Article |
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OBJECTIVETo examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with that in the salt-resistant Dahl rat.
DESIGN AND METHODSThe abundance of NOS mRNA was measured by RNase protection assay in different organs of salt-resistant and salt-sensitive Dahl rats. In addition, the zonal expression of NOS genes in the kidney under salt load and salt restriction was determined.
RESULTSThe abundance of endothelial NOS mRNA was similar between the salt-resistant and salt-sensitive Dahl rat strains in all organs. Inducible NOS mRNA was not detectable by RNase protection assay in any organ. Neuronal NOS (nNOS) mRNA expression, however, was about 50% lower in brain and kidney of salt-sensitive Dahl rats than in salt-resistant Dahl rats. Within the kidney, nNOS mRNA levels were significantly decreased in salt-sensitive Dahl rats compared with those in salt-resistant Dahl rats, in cortex, outer and inner medulla (50, 40 and 30%, respectively) under all dietary conditions. A comparison of renal nNOS gene expression in Dahl rats with that in salt-insensitive Sprague–Dawley rats revealed that the abundance of renal nNOS was similar in salt-sensitive Dahl and Sprague–Dawley rats, but was increased in salt-resistant Dahl rats relative to that in Sprague–Dawley rats.
CONCLUSIONThese data suggest that nNOS gene expression is increased in salt-resistant Dahl rats compared with that in salt-sensitive Dahl rats. This increased nNOS expression of the salt-resistant Dahl strain might play a part in compensating for a defect of renal salt excretion in the Dahl strains.</description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/00004872-200107000-00007</identifier><identifier>PMID: 11446712</identifier><identifier>CODEN: JOHYD3</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>3' Untranslated Regions - genetics ; Animals ; Arterial hypertension. Arterial hypotension ; Base Sequence - genetics ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Cardiology. Vascular system ; Diet, Sodium-Restricted ; Experimental diseases ; Gene Expression ; Kidney - physiology ; Male ; Medical sciences ; Molecular Sequence Data ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase Type I ; Rats ; Rats, Inbred Dahl - genetics ; Rats, Inbred Dahl - metabolism ; Rats, Inbred Dahl - physiology ; Rats, Sprague-Dawley - genetics ; Rats, Sprague-Dawley - metabolism ; RNA, Messenger - metabolism ; Tissue Distribution</subject><ispartof>Journal of hypertension, 2001-07, Vol.19 (7), p.1223-1231</ispartof><rights>2001 Lippincott Williams & Wilkins, Inc.</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3857-363c6900a8548a7f8e0704940d4bef440b16141340ef371ac721f92152c229813</citedby><cites>FETCH-LOGICAL-c3857-363c6900a8548a7f8e0704940d4bef440b16141340ef371ac721f92152c229813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1065354$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11446712$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Castrop, Hayo</creatorcontrib><creatorcontrib>Kurtz, Armin</creatorcontrib><title>Differential nNOS gene expression in salt-sensitive and salt-resistant Dahl rats</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>BACKGROUNDSeveral indications exist to suggest that an impaired production of nitric oxide might have a role in the development of salt-sensitive hypertension.
OBJECTIVETo examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with that in the salt-resistant Dahl rat.
DESIGN AND METHODSThe abundance of NOS mRNA was measured by RNase protection assay in different organs of salt-resistant and salt-sensitive Dahl rats. In addition, the zonal expression of NOS genes in the kidney under salt load and salt restriction was determined.
RESULTSThe abundance of endothelial NOS mRNA was similar between the salt-resistant and salt-sensitive Dahl rat strains in all organs. Inducible NOS mRNA was not detectable by RNase protection assay in any organ. Neuronal NOS (nNOS) mRNA expression, however, was about 50% lower in brain and kidney of salt-sensitive Dahl rats than in salt-resistant Dahl rats. Within the kidney, nNOS mRNA levels were significantly decreased in salt-sensitive Dahl rats compared with those in salt-resistant Dahl rats, in cortex, outer and inner medulla (50, 40 and 30%, respectively) under all dietary conditions. A comparison of renal nNOS gene expression in Dahl rats with that in salt-insensitive Sprague–Dawley rats revealed that the abundance of renal nNOS was similar in salt-sensitive Dahl and Sprague–Dawley rats, but was increased in salt-resistant Dahl rats relative to that in Sprague–Dawley rats.
CONCLUSIONThese data suggest that nNOS gene expression is increased in salt-resistant Dahl rats compared with that in salt-sensitive Dahl rats. This increased nNOS expression of the salt-resistant Dahl strain might play a part in compensating for a defect of renal salt excretion in the Dahl strains.</description><subject>3' Untranslated Regions - genetics</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Base Sequence - genetics</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Diet, Sodium-Restricted</subject><subject>Experimental diseases</subject><subject>Gene Expression</subject><subject>Kidney - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase Type I</subject><subject>Rats</subject><subject>Rats, Inbred Dahl - genetics</subject><subject>Rats, Inbred Dahl - metabolism</subject><subject>Rats, Inbred Dahl - physiology</subject><subject>Rats, Sprague-Dawley - genetics</subject><subject>Rats, Sprague-Dawley - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Tissue Distribution</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kV1PVDEQhhsigQX8C6YXxruD_TxtLw0gmBAxAa6b7tmpW-32rJ2zAv_e4q7Kjb2Z9M0zM-lTQihnp5w58561o6wRnWCMM9Nu3XNk9siMKyM7rZ19RWZM9LLrpRaH5AjxWyOsM_KAHHKuVG-4mJEv5ylGqFCmFDItn29u6VcoQOFxXQExjYWmQjHkqUMomKb0E2goi23UkIRTKBM9D8tMa5jwhOzHkBFe7-oxuf94cXd21V3fXH46-3DdDdJq08leDr1jLFitbDDRQnuGcoot1ByiUmzOe664VAyiNDwMRvDoBNdiEMJZLo_Ju-3cdR1_bAAnv0o4QM6hwLhBb5hzTPeygXYLDnVErBD9uqZVqE-eM_9s0_-x6f_a_B2Z1vpmt2MzX8HiX-NOXwPe7oCAQ8ixhjIkfLGg11Krhqkt9jDmCSp-z5sHqH4JzeHS_-8z5S-pRYn9</recordid><startdate>200107</startdate><enddate>200107</enddate><creator>Castrop, Hayo</creator><creator>Kurtz, Armin</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</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>7X8</scope></search><sort><creationdate>200107</creationdate><title>Differential nNOS gene expression in salt-sensitive and salt-resistant Dahl rats</title><author>Castrop, Hayo ; Kurtz, Armin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3857-363c6900a8548a7f8e0704940d4bef440b16141340ef371ac721f92152c229813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>3' Untranslated Regions - genetics</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Base Sequence - genetics</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Cardiology. Vascular system</topic><topic>Diet, Sodium-Restricted</topic><topic>Experimental diseases</topic><topic>Gene Expression</topic><topic>Kidney - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase Type I</topic><topic>Rats</topic><topic>Rats, Inbred Dahl - genetics</topic><topic>Rats, Inbred Dahl - metabolism</topic><topic>Rats, Inbred Dahl - physiology</topic><topic>Rats, Sprague-Dawley - genetics</topic><topic>Rats, Sprague-Dawley - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Tissue Distribution</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Castrop, Hayo</creatorcontrib><creatorcontrib>Kurtz, Armin</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>MEDLINE - Academic</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Castrop, Hayo</au><au>Kurtz, Armin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential nNOS gene expression in salt-sensitive and salt-resistant Dahl rats</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2001-07</date><risdate>2001</risdate><volume>19</volume><issue>7</issue><spage>1223</spage><epage>1231</epage><pages>1223-1231</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><coden>JOHYD3</coden><abstract>BACKGROUNDSeveral indications exist to suggest that an impaired production of nitric oxide might have a role in the development of salt-sensitive hypertension.
OBJECTIVETo examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with that in the salt-resistant Dahl rat.
DESIGN AND METHODSThe abundance of NOS mRNA was measured by RNase protection assay in different organs of salt-resistant and salt-sensitive Dahl rats. In addition, the zonal expression of NOS genes in the kidney under salt load and salt restriction was determined.
RESULTSThe abundance of endothelial NOS mRNA was similar between the salt-resistant and salt-sensitive Dahl rat strains in all organs. Inducible NOS mRNA was not detectable by RNase protection assay in any organ. Neuronal NOS (nNOS) mRNA expression, however, was about 50% lower in brain and kidney of salt-sensitive Dahl rats than in salt-resistant Dahl rats. Within the kidney, nNOS mRNA levels were significantly decreased in salt-sensitive Dahl rats compared with those in salt-resistant Dahl rats, in cortex, outer and inner medulla (50, 40 and 30%, respectively) under all dietary conditions. A comparison of renal nNOS gene expression in Dahl rats with that in salt-insensitive Sprague–Dawley rats revealed that the abundance of renal nNOS was similar in salt-sensitive Dahl and Sprague–Dawley rats, but was increased in salt-resistant Dahl rats relative to that in Sprague–Dawley rats.
CONCLUSIONThese data suggest that nNOS gene expression is increased in salt-resistant Dahl rats compared with that in salt-sensitive Dahl rats. This increased nNOS expression of the salt-resistant Dahl strain might play a part in compensating for a defect of renal salt excretion in the Dahl strains.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>11446712</pmid><doi>10.1097/00004872-200107000-00007</doi><tpages>9</tpages></addata></record> |
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| subjects | 3' Untranslated Regions - genetics Animals Arterial hypertension. Arterial hypotension Base Sequence - genetics Biological and medical sciences Blood and lymphatic vessels Blood Pressure Cardiology. Vascular system Diet, Sodium-Restricted Experimental diseases Gene Expression Kidney - physiology Male Medical sciences Molecular Sequence Data Nitric Oxide Synthase - genetics Nitric Oxide Synthase Type I Rats Rats, Inbred Dahl - genetics Rats, Inbred Dahl - metabolism Rats, Inbred Dahl - physiology Rats, Sprague-Dawley - genetics Rats, Sprague-Dawley - metabolism RNA, Messenger - metabolism Tissue Distribution |
| title | Differential nNOS gene expression in salt-sensitive and salt-resistant Dahl rats |
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