Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity
Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity. Increasing evidence suggests that angiotensin-(1–7) [Ang-(1–7)] acts as an endogenous antagonist of Ang II when the renin-angiotensin system (RAS) is activated. In the present study, we therefor...
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| Veröffentlicht in: | Kidney international 2005-04, Vol.67 (4), p.1453-1461 |
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| creator | Bürgelová, Marcela Kramer, Herbert J. Teplan, Vladimír Thumová, Monika Červenka, Luděk |
| description | Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity.
Increasing evidence suggests that angiotensin-(1–7) [Ang-(1–7)] acts as an endogenous antagonist of Ang II when the renin-angiotensin system (RAS) is activated. In the present study, we therefore compared the effects of acute intrarenal (i.r.) Ang-(1–7) receptor blockade on renal function under conditions of normal and increased intrarenal Ang II concentration.
Salt-replete Hannover-Sprague Dawley rats (HanSD) served as control animals. As models with enhanced action of Ang II we first used transgenic rats harboring the Ren-2 renin gene (TGR), second, Ang II-infused rats, third, 2-kidney, 1-clip (2K1C) hypertensive rats on normal salt intake, and fourth, salt-depleted TGR and HanSD.
I.r. Ang-(1–7) receptor blockade elicited significant decreases in glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion in 2K1C rats, and in salt-depleted TGR and HanSD. In contrast, i.r. Ang-(1–7) receptor blockade did not significantly change GFR, RPF, and sodium excretion in salt-replete TGR and HanSD, or in Ang II-infused rats.
These findings suggest that under conditions of normal intrarenal RAS activity and increased intrarenal Ang II action by infusion of Ang II or by insertion of a renin gene in salt-replete conditions, Ang-(1–7) is not an important factor in the regulation of renal function. In contrast, under conditions of endogenous RAS activation due to clipping of the renal artery or to sodium restriction, Ang-(1–7) serves as opponent of the vasoconstrictor actions of Ang II. |
| doi_str_mv | 10.1111/j.1523-1755.2005.00222.x |
| format | Article |
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Increasing evidence suggests that angiotensin-(1–7) [Ang-(1–7)] acts as an endogenous antagonist of Ang II when the renin-angiotensin system (RAS) is activated. In the present study, we therefore compared the effects of acute intrarenal (i.r.) Ang-(1–7) receptor blockade on renal function under conditions of normal and increased intrarenal Ang II concentration.
Salt-replete Hannover-Sprague Dawley rats (HanSD) served as control animals. As models with enhanced action of Ang II we first used transgenic rats harboring the Ren-2 renin gene (TGR), second, Ang II-infused rats, third, 2-kidney, 1-clip (2K1C) hypertensive rats on normal salt intake, and fourth, salt-depleted TGR and HanSD.
I.r. Ang-(1–7) receptor blockade elicited significant decreases in glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion in 2K1C rats, and in salt-depleted TGR and HanSD. In contrast, i.r. Ang-(1–7) receptor blockade did not significantly change GFR, RPF, and sodium excretion in salt-replete TGR and HanSD, or in Ang II-infused rats.
These findings suggest that under conditions of normal intrarenal RAS activity and increased intrarenal Ang II action by infusion of Ang II or by insertion of a renin gene in salt-replete conditions, Ang-(1–7) is not an important factor in the regulation of renal function. In contrast, under conditions of endogenous RAS activation due to clipping of the renal artery or to sodium restriction, Ang-(1–7) serves as opponent of the vasoconstrictor actions of Ang II.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1111/j.1523-1755.2005.00222.x</identifier><identifier>PMID: 15780097</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Angiotensin I - pharmacology ; angiotensin II ; Angiotensin II - pharmacology ; Angiotensin II - physiology ; angiotensin-(1–7) ; Animals ; Animals, Genetically Modified ; Biological and medical sciences ; Diuresis - drug effects ; Glomerular Filtration Rate - drug effects ; Glomerular Filtration Rate - physiology ; hypertension ; Kidney - drug effects ; Kidney - physiology ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Peptide Fragments - pharmacology ; Rats ; Rats, Sprague-Dawley ; renal function ; Renin-Angiotensin System</subject><ispartof>Kidney international, 2005-04, Vol.67 (4), p.1453-1461</ispartof><rights>2005 International Society of Nephrology</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-146406b51e268ecee7c5a3e0d7abc86caa69c96d60db46c92263ca70c4e605cd3</citedby><cites>FETCH-LOGICAL-c479t-146406b51e268ecee7c5a3e0d7abc86caa69c96d60db46c92263ca70c4e605cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16661613$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15780097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bürgelová, Marcela</creatorcontrib><creatorcontrib>Kramer, Herbert J.</creatorcontrib><creatorcontrib>Teplan, Vladimír</creatorcontrib><creatorcontrib>Thumová, Monika</creatorcontrib><creatorcontrib>Červenka, Luděk</creatorcontrib><title>Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity.
Increasing evidence suggests that angiotensin-(1–7) [Ang-(1–7)] acts as an endogenous antagonist of Ang II when the renin-angiotensin system (RAS) is activated. In the present study, we therefore compared the effects of acute intrarenal (i.r.) Ang-(1–7) receptor blockade on renal function under conditions of normal and increased intrarenal Ang II concentration.
Salt-replete Hannover-Sprague Dawley rats (HanSD) served as control animals. As models with enhanced action of Ang II we first used transgenic rats harboring the Ren-2 renin gene (TGR), second, Ang II-infused rats, third, 2-kidney, 1-clip (2K1C) hypertensive rats on normal salt intake, and fourth, salt-depleted TGR and HanSD.
I.r. Ang-(1–7) receptor blockade elicited significant decreases in glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion in 2K1C rats, and in salt-depleted TGR and HanSD. In contrast, i.r. Ang-(1–7) receptor blockade did not significantly change GFR, RPF, and sodium excretion in salt-replete TGR and HanSD, or in Ang II-infused rats.
These findings suggest that under conditions of normal intrarenal RAS activity and increased intrarenal Ang II action by infusion of Ang II or by insertion of a renin gene in salt-replete conditions, Ang-(1–7) is not an important factor in the regulation of renal function. In contrast, under conditions of endogenous RAS activation due to clipping of the renal artery or to sodium restriction, Ang-(1–7) serves as opponent of the vasoconstrictor actions of Ang II.</description><subject>Angiotensin I - pharmacology</subject><subject>angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Angiotensin II - physiology</subject><subject>angiotensin-(1–7)</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Biological and medical sciences</subject><subject>Diuresis - drug effects</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Glomerular Filtration Rate - physiology</subject><subject>hypertension</subject><subject>Kidney - drug effects</subject><subject>Kidney - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Peptide Fragments - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>renal function</subject><subject>Renin-Angiotensin System</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkcFu1DAQhi0EokvhFZCFRAWHhLFjO8mxVAVWqsQFzpbjTFqHrF3spLS3vgNvyJPgsCsqccEXa2a-fzT6f0Iog5Ll924smeRVwWopSw4gSwDOeXn7iGz-Dh6TDUAjCy6r5og8S2mEXLcVPCVHTNYNQFtvyHg-DGjnRMNAjb90YUafnC_esF_3P-u3tJuC_WZ6pMHTiN5MdFi8nV0uXe6YrPzh5iuK_sp4i33uztHsyVN_SbdbajJ-4-a75-TJYKaELw7_Mfn64fzL2afi4vPH7dnpRWFF3c4FE0qA6iRDrhq0iLWVpkLoa9PZRlljVGtb1SvoO6Fsy7mqrKnBClQgbV8dk5P93usYvi-YZr1zyeI0GY9hSVrVUjApmgy--gccwxLz5UlzBkw0QsoMNXvIxpBSxEFfR7cz8U4z0GsYetSr53r1XK9h6D9h6NssfXnYv3Q77B-EB_cz8PoAmGTNNMRsoUsPnFKKKVZl7v2ew2zbjcOok3W42u1iDk_3wf3_mt9zDKhl</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Bürgelová, Marcela</creator><creator>Kramer, Herbert J.</creator><creator>Teplan, Vladimír</creator><creator>Thumová, Monika</creator><creator>Červenka, Luděk</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</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>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20050401</creationdate><title>Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity</title><author>Bürgelová, Marcela ; Kramer, Herbert J. ; Teplan, Vladimír ; Thumová, Monika ; Červenka, Luděk</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-146406b51e268ecee7c5a3e0d7abc86caa69c96d60db46c92263ca70c4e605cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Angiotensin I - pharmacology</topic><topic>angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Angiotensin II - physiology</topic><topic>angiotensin-(1–7)</topic><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Biological and medical sciences</topic><topic>Diuresis - drug effects</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Glomerular Filtration Rate - physiology</topic><topic>hypertension</topic><topic>Kidney - drug effects</topic><topic>Kidney - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Peptide Fragments - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>renal function</topic><topic>Renin-Angiotensin System</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bürgelová, Marcela</creatorcontrib><creatorcontrib>Kramer, Herbert J.</creatorcontrib><creatorcontrib>Teplan, Vladimír</creatorcontrib><creatorcontrib>Thumová, Monika</creatorcontrib><creatorcontrib>Červenka, Luděk</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>Nursing & Allied Health Premium</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><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bürgelová, Marcela</au><au>Kramer, Herbert J.</au><au>Teplan, Vladimír</au><au>Thumová, Monika</au><au>Červenka, Luděk</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>67</volume><issue>4</issue><spage>1453</spage><epage>1461</epage><pages>1453-1461</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity.
Increasing evidence suggests that angiotensin-(1–7) [Ang-(1–7)] acts as an endogenous antagonist of Ang II when the renin-angiotensin system (RAS) is activated. In the present study, we therefore compared the effects of acute intrarenal (i.r.) Ang-(1–7) receptor blockade on renal function under conditions of normal and increased intrarenal Ang II concentration.
Salt-replete Hannover-Sprague Dawley rats (HanSD) served as control animals. As models with enhanced action of Ang II we first used transgenic rats harboring the Ren-2 renin gene (TGR), second, Ang II-infused rats, third, 2-kidney, 1-clip (2K1C) hypertensive rats on normal salt intake, and fourth, salt-depleted TGR and HanSD.
I.r. Ang-(1–7) receptor blockade elicited significant decreases in glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion in 2K1C rats, and in salt-depleted TGR and HanSD. In contrast, i.r. Ang-(1–7) receptor blockade did not significantly change GFR, RPF, and sodium excretion in salt-replete TGR and HanSD, or in Ang II-infused rats.
These findings suggest that under conditions of normal intrarenal RAS activity and increased intrarenal Ang II action by infusion of Ang II or by insertion of a renin gene in salt-replete conditions, Ang-(1–7) is not an important factor in the regulation of renal function. In contrast, under conditions of endogenous RAS activation due to clipping of the renal artery or to sodium restriction, Ang-(1–7) serves as opponent of the vasoconstrictor actions of Ang II.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15780097</pmid><doi>10.1111/j.1523-1755.2005.00222.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin I - pharmacology angiotensin II Angiotensin II - pharmacology Angiotensin II - physiology angiotensin-(1–7) Animals Animals, Genetically Modified Biological and medical sciences Diuresis - drug effects Glomerular Filtration Rate - drug effects Glomerular Filtration Rate - physiology hypertension Kidney - drug effects Kidney - physiology Male Medical sciences Nephrology. Urinary tract diseases Peptide Fragments - pharmacology Rats Rats, Sprague-Dawley renal function Renin-Angiotensin System |
| title | Effects of angiotensin-(1–7) blockade on renal function in rats with enhanced intrarenal Ang II activity |
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