Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure
Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acid...
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| Veröffentlicht in: | Kidney & blood pressure research 2019-08, Vol.44 (4), p.792-809 |
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| creator | Vacková, Šárka Kikerlová, Soňa Melenovsky, Vojtěch Kolář, František Imig, John D. Kompanowska-Jezierska, Elzbieta Sadowski, Janusz Červenka, Luděk |
| description | Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs). Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF. |
| doi_str_mv | 10.1159/000501688 |
| format | Article |
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Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.</description><identifier>ISSN: 1420-4096</identifier><identifier>EISSN: 1423-0143</identifier><identifier>DOI: 10.1159/000501688</identifier><identifier>PMID: 31430751</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acetylcholine ; Angiotensin ; Angiotensin II ; Angiotensin II - adverse effects ; Angiotensins ; Animals ; Aorto-caval fistula ; Arterio-Arterial Fistula - physiopathology ; Blood flow ; Blood pressure ; Bradykinin ; Cardiovascular agents ; Congestive heart failure ; Coronary vessels ; Drug therapy ; Endothelium ; Epoxyeicosatrienoic acid ; Fistula ; Fistulae ; Fistulas ; Genetic engineering ; Heart ; Heart failure ; Heart Failure - complications ; Heart Failure - physiopathology ; Hemodynamics ; Hypertension ; Hypertension - chemically induced ; Hypertension - complications ; Kidneys ; Laboratory animals ; Medical prognosis ; Nitric oxide ; Norepinephrine ; Peptides ; Physiological aspects ; Pulmonary Artery - abnormalities ; Pulmonary Artery - physiopathology ; Rats ; Rats, Transgenic ; Renal artery ; Renal blood flow ; Renal Circulation - drug effects ; Renal dysfunction ; Renal function ; Renal vascular reactivity ; Research Article ; Rodents ; Testing ; Vasoactive agents ; Vasoconstriction - drug effects ; Vasoconstrictor Agents - pharmacology ; Vasodilation ; Vasodilation - drug effects ; Vasodilator agents</subject><ispartof>Kidney & blood pressure research, 2019-08, Vol.44 (4), p.792-809</ispartof><rights>2019 The Author(s) Published by S. Karger AG, Basel</rights><rights>2019 The Author(s) Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2019 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c586t-3f34fcda1b5304f4cfd80a5771dc0f01408ce1e62790f17a85ca79e1478429453</citedby><cites>FETCH-LOGICAL-c586t-3f34fcda1b5304f4cfd80a5771dc0f01408ce1e62790f17a85ca79e1478429453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,860,881,2095,27614,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31430751$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vacková, Šárka</creatorcontrib><creatorcontrib>Kikerlová, Soňa</creatorcontrib><creatorcontrib>Melenovsky, Vojtěch</creatorcontrib><creatorcontrib>Kolář, František</creatorcontrib><creatorcontrib>Imig, John D.</creatorcontrib><creatorcontrib>Kompanowska-Jezierska, Elzbieta</creatorcontrib><creatorcontrib>Sadowski, Janusz</creatorcontrib><creatorcontrib>Červenka, Luděk</creatorcontrib><title>Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure</title><title>Kidney & blood pressure research</title><addtitle>Kidney Blood Press Res</addtitle><description>Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs). Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.</description><subject>Acetylcholine</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - adverse effects</subject><subject>Angiotensins</subject><subject>Animals</subject><subject>Aorto-caval fistula</subject><subject>Arterio-Arterial Fistula - physiopathology</subject><subject>Blood flow</subject><subject>Blood pressure</subject><subject>Bradykinin</subject><subject>Cardiovascular agents</subject><subject>Congestive heart failure</subject><subject>Coronary vessels</subject><subject>Drug therapy</subject><subject>Endothelium</subject><subject>Epoxyeicosatrienoic acid</subject><subject>Fistula</subject><subject>Fistulae</subject><subject>Fistulas</subject><subject>Genetic engineering</subject><subject>Heart</subject><subject>Heart failure</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - physiopathology</subject><subject>Hemodynamics</subject><subject>Hypertension</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - complications</subject><subject>Kidneys</subject><subject>Laboratory animals</subject><subject>Medical prognosis</subject><subject>Nitric oxide</subject><subject>Norepinephrine</subject><subject>Peptides</subject><subject>Physiological aspects</subject><subject>Pulmonary Artery - abnormalities</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Rats</subject><subject>Rats, Transgenic</subject><subject>Renal artery</subject><subject>Renal blood flow</subject><subject>Renal Circulation - drug effects</subject><subject>Renal dysfunction</subject><subject>Renal function</subject><subject>Renal vascular reactivity</subject><subject>Research Article</subject><subject>Rodents</subject><subject>Testing</subject><subject>Vasoactive agents</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vasodilation</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator agents</subject><issn>1420-4096</issn><issn>1423-0143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptksGO0zAQhiMEYpeFA3eELHHikMVOHCc5oVJYWrESUgVcLdceZ11SO9jpon0FnpppUworIR_Gnvnn84w9Wfac0UvGqvYNpbSiTDTNg-yc8aLMKePlw8Oe5py24ix7ktLmIKPF4-ysxDitK3ae_Zr1I0QwZAVe9eSbSnrXq4jHNASf3C14SImMYR8KSo_oIbMO_JiI82Sl0P504w2Z-c6FETDFk-Uyfw8DeIMysrgbIB4CwRPlDZkH30E6gBag4kiulOt3EZ5mj6zqEzw72ovs69WHL_NFfv3543I-u8511YgxL23JrTaKrauScsu1NQ1VVV0zo6nFzmmjgYEo6pZaVqum0qpugfG64UXLq_IiW05cE9RGDtFtVbyTQTl5cITYSazK6R5kI2hbCA3crhvOWtVqaPF2AwXXwgiLrLcTa9itt2A0NhxVfw96P-LdjezCrWSU0ZrWBRJeHQkx_Njhu8hN2EX8iySLEj-sYUy0qLqcVJ3Cspy3AWkal4Gt08GDdeifCcqqiolaYMLrKUHHkFIEe6qJUbkfGnkaGtS-_LeJk_LPlPyt8buKHcST4NO71YSQg9m_xYv_qo63_AZrddKK</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Vacková, Šárka</creator><creator>Kikerlová, Soňa</creator><creator>Melenovsky, Vojtěch</creator><creator>Kolář, František</creator><creator>Imig, John D.</creator><creator>Kompanowska-Jezierska, Elzbieta</creator><creator>Sadowski, Janusz</creator><creator>Červenka, Luděk</creator><general>S. Karger AG</general><general>Karger Publishers</general><scope>M--</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>IAO</scope><scope>3V.</scope><scope>7QL</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>S0X</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20190801</creationdate><title>Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure</title><author>Vacková, Šárka ; Kikerlová, Soňa ; Melenovsky, Vojtěch ; Kolář, František ; Imig, John D. ; Kompanowska-Jezierska, Elzbieta ; Sadowski, Janusz ; Červenka, Luděk</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c586t-3f34fcda1b5304f4cfd80a5771dc0f01408ce1e62790f17a85ca79e1478429453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acetylcholine</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - adverse effects</topic><topic>Angiotensins</topic><topic>Animals</topic><topic>Aorto-caval fistula</topic><topic>Arterio-Arterial Fistula - physiopathology</topic><topic>Blood flow</topic><topic>Blood pressure</topic><topic>Bradykinin</topic><topic>Cardiovascular agents</topic><topic>Congestive heart failure</topic><topic>Coronary vessels</topic><topic>Drug therapy</topic><topic>Endothelium</topic><topic>Epoxyeicosatrienoic acid</topic><topic>Fistula</topic><topic>Fistulae</topic><topic>Fistulas</topic><topic>Genetic engineering</topic><topic>Heart</topic><topic>Heart failure</topic><topic>Heart Failure - complications</topic><topic>Heart Failure - physiopathology</topic><topic>Hemodynamics</topic><topic>Hypertension</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - complications</topic><topic>Kidneys</topic><topic>Laboratory animals</topic><topic>Medical prognosis</topic><topic>Nitric oxide</topic><topic>Norepinephrine</topic><topic>Peptides</topic><topic>Physiological aspects</topic><topic>Pulmonary Artery - abnormalities</topic><topic>Pulmonary Artery - physiopathology</topic><topic>Rats</topic><topic>Rats, Transgenic</topic><topic>Renal artery</topic><topic>Renal blood flow</topic><topic>Renal Circulation - drug effects</topic><topic>Renal dysfunction</topic><topic>Renal function</topic><topic>Renal vascular reactivity</topic><topic>Research Article</topic><topic>Rodents</topic><topic>Testing</topic><topic>Vasoactive agents</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vasodilation</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vacková, Šárka</creatorcontrib><creatorcontrib>Kikerlová, Soňa</creatorcontrib><creatorcontrib>Melenovsky, Vojtěch</creatorcontrib><creatorcontrib>Kolář, František</creatorcontrib><creatorcontrib>Imig, John D.</creatorcontrib><creatorcontrib>Kompanowska-Jezierska, Elzbieta</creatorcontrib><creatorcontrib>Sadowski, Janusz</creatorcontrib><creatorcontrib>Červenka, Luděk</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</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>Technology Research Database</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>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</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>SIRS Editorial</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Kidney & blood pressure research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vacková, Šárka</au><au>Kikerlová, Soňa</au><au>Melenovsky, Vojtěch</au><au>Kolář, František</au><au>Imig, John D.</au><au>Kompanowska-Jezierska, Elzbieta</au><au>Sadowski, Janusz</au><au>Červenka, Luděk</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure</atitle><jtitle>Kidney & blood pressure research</jtitle><addtitle>Kidney Blood Press Res</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>44</volume><issue>4</issue><spage>792</spage><epage>809</epage><pages>792-809</pages><issn>1420-4096</issn><eissn>1423-0143</eissn><abstract>Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs). Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>31430751</pmid><doi>10.1159/000501688</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney & blood pressure research, 2019-08, Vol.44 (4), p.792-809 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Karger Open Access |
| subjects | Acetylcholine Angiotensin Angiotensin II Angiotensin II - adverse effects Angiotensins Animals Aorto-caval fistula Arterio-Arterial Fistula - physiopathology Blood flow Blood pressure Bradykinin Cardiovascular agents Congestive heart failure Coronary vessels Drug therapy Endothelium Epoxyeicosatrienoic acid Fistula Fistulae Fistulas Genetic engineering Heart Heart failure Heart Failure - complications Heart Failure - physiopathology Hemodynamics Hypertension Hypertension - chemically induced Hypertension - complications Kidneys Laboratory animals Medical prognosis Nitric oxide Norepinephrine Peptides Physiological aspects Pulmonary Artery - abnormalities Pulmonary Artery - physiopathology Rats Rats, Transgenic Renal artery Renal blood flow Renal Circulation - drug effects Renal dysfunction Renal function Renal vascular reactivity Research Article Rodents Testing Vasoactive agents Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology Vasodilation Vasodilation - drug effects Vasodilator agents |
| title | Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure |
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