Endothelin ETA receptor-subtype specific antagonism does not mitigate the acute systemic or renal effects of exogenous angiotensin II in humans
Background Angiotensin II (Ang II) is assumed to play a pathophysiological role in a variety of vascular diseases. Animal studies indicate that these effects are partly attributed to stimulation of endothelin‐1 (ET‐1) release. The aim of the present study was to investigate whether the acute effects...
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| Veröffentlicht in: | European journal of clinical investigation 2002-04, Vol.32 (4), p.230-235 |
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| creator | Bayerle-Eder, M. Langenberger, H. Pleiner, J. Polska, E. Mensik, C. Eichler, H.-G. Wolzt, M. Schmetterer, L. |
| description | Background Angiotensin II (Ang II) is assumed to play a pathophysiological role in a variety of vascular diseases. Animal studies indicate that these effects are partly attributed to stimulation of endothelin‐1 (ET‐1) release. The aim of the present study was to investigate whether the acute effects of Ang II on systemic and renal haemodynamics in healthy subjects can be influenced by endothelin ETA‐receptor blockade.
Design The study design was balanced, randomized, placebo‐controlled, double blind, two‐way cross‐over, in 10 healthy male subjects.
Methods Subjects received stepwise increasing intravenous doses of Ang II (0·65, 1·25, 2·5, 5 ng kg−1 min−1 for 15 min per dose level) in the presence or absence of BQ‐123 (60 µg min−1), a specific ETA‐receptor antagonist. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by the para‐aminohippurate and inulin plasma clearance method, respectively. Renal vascular resistance (RVR) was calculated from mean arterial pressure (MAP) and renal plasma flow.
Results Ang II decreased RPF by 34% and GFR by 9% and increased RVR by 94% and MAP by 27% (ANOVA, P |
| doi_str_mv | 10.1046/j.1365-2362.2002.00974.x |
| format | Article |
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Design The study design was balanced, randomized, placebo‐controlled, double blind, two‐way cross‐over, in 10 healthy male subjects.
Methods Subjects received stepwise increasing intravenous doses of Ang II (0·65, 1·25, 2·5, 5 ng kg−1 min−1 for 15 min per dose level) in the presence or absence of BQ‐123 (60 µg min−1), a specific ETA‐receptor antagonist. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by the para‐aminohippurate and inulin plasma clearance method, respectively. Renal vascular resistance (RVR) was calculated from mean arterial pressure (MAP) and renal plasma flow.
Results Ang II decreased RPF by 34% and GFR by 9% and increased RVR by 94% and MAP by 27% (ANOVA, P < 0·001 vs. baseline, for all parameters). BQ‐123 did not alter these renal and systemic haemodynamic responses to a significant degree. In addition, BQ‐123 had no significant haemodynamic effect under baseline conditions.
Conclusions Short‐term increase of circulating Ang II levels causes systemic and renal pressor effects, which are not mitigated by endothelin ETA‐receptor blockade. This suggests that the pressor response to Ang II cannot be accounted for by the acute release of vasoactive ET‐1.</description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1046/j.1365-2362.2002.00974.x</identifier><identifier>PMID: 11952807</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adult ; Angiotensin ; Angiotensin II - pharmacology ; Biological and medical sciences ; Cardiovascular system ; Cross-Over Studies ; Double-Blind Method ; endothelial function ; endothelial receptors ; Endothelin Receptor Antagonists ; Endothelin-1 - physiology ; endothelins ; Glomerular Filtration Rate - drug effects ; haemodynamics ; Hemodynamics - drug effects ; Humans ; Inulin ; Male ; Medical sciences ; Miscellaneous ; p-Aminohippuric Acid ; Peptides, Cyclic - pharmacology ; Pharmacology. Drug treatments ; Renal Circulation - drug effects ; Renal Plasma Flow - drug effects ; Vascular Resistance - drug effects</subject><ispartof>European journal of clinical investigation, 2002-04, Vol.32 (4), p.230-235</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4324-52744e8ec7c856e7023ef71ee1df752109c64b937f2e5cce4484efd98e9d2c2c3</citedby><cites>FETCH-LOGICAL-c4324-52744e8ec7c856e7023ef71ee1df752109c64b937f2e5cce4484efd98e9d2c2c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2362.2002.00974.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2362.2002.00974.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13623777$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11952807$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bayerle-Eder, M.</creatorcontrib><creatorcontrib>Langenberger, H.</creatorcontrib><creatorcontrib>Pleiner, J.</creatorcontrib><creatorcontrib>Polska, E.</creatorcontrib><creatorcontrib>Mensik, C.</creatorcontrib><creatorcontrib>Eichler, H.-G.</creatorcontrib><creatorcontrib>Wolzt, M.</creatorcontrib><creatorcontrib>Schmetterer, L.</creatorcontrib><title>Endothelin ETA receptor-subtype specific antagonism does not mitigate the acute systemic or renal effects of exogenous angiotensin II in humans</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description>Background Angiotensin II (Ang II) is assumed to play a pathophysiological role in a variety of vascular diseases. Animal studies indicate that these effects are partly attributed to stimulation of endothelin‐1 (ET‐1) release. The aim of the present study was to investigate whether the acute effects of Ang II on systemic and renal haemodynamics in healthy subjects can be influenced by endothelin ETA‐receptor blockade.
Design The study design was balanced, randomized, placebo‐controlled, double blind, two‐way cross‐over, in 10 healthy male subjects.
Methods Subjects received stepwise increasing intravenous doses of Ang II (0·65, 1·25, 2·5, 5 ng kg−1 min−1 for 15 min per dose level) in the presence or absence of BQ‐123 (60 µg min−1), a specific ETA‐receptor antagonist. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by the para‐aminohippurate and inulin plasma clearance method, respectively. Renal vascular resistance (RVR) was calculated from mean arterial pressure (MAP) and renal plasma flow.
Results Ang II decreased RPF by 34% and GFR by 9% and increased RVR by 94% and MAP by 27% (ANOVA, P < 0·001 vs. baseline, for all parameters). BQ‐123 did not alter these renal and systemic haemodynamic responses to a significant degree. In addition, BQ‐123 had no significant haemodynamic effect under baseline conditions.
Conclusions Short‐term increase of circulating Ang II levels causes systemic and renal pressor effects, which are not mitigated by endothelin ETA‐receptor blockade. This suggests that the pressor response to Ang II cannot be accounted for by the acute release of vasoactive ET‐1.</description><subject>Adult</subject><subject>Angiotensin</subject><subject>Angiotensin II - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cardiovascular system</subject><subject>Cross-Over Studies</subject><subject>Double-Blind Method</subject><subject>endothelial function</subject><subject>endothelial receptors</subject><subject>Endothelin Receptor Antagonists</subject><subject>Endothelin-1 - physiology</subject><subject>endothelins</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>haemodynamics</subject><subject>Hemodynamics - drug effects</subject><subject>Humans</subject><subject>Inulin</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>p-Aminohippuric Acid</subject><subject>Peptides, Cyclic - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Renal Circulation - drug effects</subject><subject>Renal Plasma Flow - drug effects</subject><subject>Vascular Resistance - drug effects</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc-O0zAQxiMEYsvCKyBf4Jbgf4kTicuqdJei1SKhRRwt1xl3XRK72I5on4JXxqHV7pWLPdL8vm9G8xUFIrgimDcfdhVhTV1S1tCKYkwrjDvBq8OzYvHYeF4sMCa8pJ2gF8WrGHcY45Yw-rK4IKSraYvFovizcr1PDzBYh1b3VyiAhn3yoYzTJh33gOIetDVWI-WS2npn44h6DxE5n9Bok92qBCg7IKWnXMVjTDBm3ods5tSAwBjQKSJvEBz8FpyfYnbbWp_AxTx3vUb5fZhG5eLr4oVRQ4Q35_-y-H69ul9-Lm-_3qyXV7el5ozysqaCc2hBC93WDQhMGRhBAEhvRE0J7nTDNx0ThkKtNXDecjB910LXU001uyzen3z3wf-aICY52qhhGJSDvJ8UpMGkJiSD7QnUwccYwMh9sKMKR0mwnMOQOznfXM43l3MY8l8Y8pClb88zps0I_ZPwfP0MvDsDKmo1mKCctvGJy45MiJn7eOJ-2wGO_72AXC3Xucjy8iS3OZrDo1yFn7IRTNTyx92NvLv-xrpPLZFf2F-Ykral</recordid><startdate>200204</startdate><enddate>200204</enddate><creator>Bayerle-Eder, M.</creator><creator>Langenberger, H.</creator><creator>Pleiner, J.</creator><creator>Polska, E.</creator><creator>Mensik, C.</creator><creator>Eichler, H.-G.</creator><creator>Wolzt, M.</creator><creator>Schmetterer, L.</creator><general>Blackwell Science Ltd</general><general>Blackwell</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>7X8</scope></search><sort><creationdate>200204</creationdate><title>Endothelin ETA receptor-subtype specific antagonism does not mitigate the acute systemic or renal effects of exogenous angiotensin II in humans</title><author>Bayerle-Eder, M. ; Langenberger, H. ; Pleiner, J. ; Polska, E. ; Mensik, C. ; Eichler, H.-G. ; Wolzt, M. ; Schmetterer, L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4324-52744e8ec7c856e7023ef71ee1df752109c64b937f2e5cce4484efd98e9d2c2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Angiotensin</topic><topic>Angiotensin II - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cardiovascular system</topic><topic>Cross-Over Studies</topic><topic>Double-Blind Method</topic><topic>endothelial function</topic><topic>endothelial receptors</topic><topic>Endothelin Receptor Antagonists</topic><topic>Endothelin-1 - physiology</topic><topic>endothelins</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>haemodynamics</topic><topic>Hemodynamics - drug effects</topic><topic>Humans</topic><topic>Inulin</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>p-Aminohippuric Acid</topic><topic>Peptides, Cyclic - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Renal Circulation - drug effects</topic><topic>Renal Plasma Flow - drug effects</topic><topic>Vascular Resistance - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bayerle-Eder, M.</creatorcontrib><creatorcontrib>Langenberger, H.</creatorcontrib><creatorcontrib>Pleiner, J.</creatorcontrib><creatorcontrib>Polska, E.</creatorcontrib><creatorcontrib>Mensik, C.</creatorcontrib><creatorcontrib>Eichler, H.-G.</creatorcontrib><creatorcontrib>Wolzt, M.</creatorcontrib><creatorcontrib>Schmetterer, L.</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>MEDLINE - Academic</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bayerle-Eder, M.</au><au>Langenberger, H.</au><au>Pleiner, J.</au><au>Polska, E.</au><au>Mensik, C.</au><au>Eichler, H.-G.</au><au>Wolzt, M.</au><au>Schmetterer, L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelin ETA receptor-subtype specific antagonism does not mitigate the acute systemic or renal effects of exogenous angiotensin II in humans</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2002-04</date><risdate>2002</risdate><volume>32</volume><issue>4</issue><spage>230</spage><epage>235</epage><pages>230-235</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract>Background Angiotensin II (Ang II) is assumed to play a pathophysiological role in a variety of vascular diseases. Animal studies indicate that these effects are partly attributed to stimulation of endothelin‐1 (ET‐1) release. The aim of the present study was to investigate whether the acute effects of Ang II on systemic and renal haemodynamics in healthy subjects can be influenced by endothelin ETA‐receptor blockade.
Design The study design was balanced, randomized, placebo‐controlled, double blind, two‐way cross‐over, in 10 healthy male subjects.
Methods Subjects received stepwise increasing intravenous doses of Ang II (0·65, 1·25, 2·5, 5 ng kg−1 min−1 for 15 min per dose level) in the presence or absence of BQ‐123 (60 µg min−1), a specific ETA‐receptor antagonist. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by the para‐aminohippurate and inulin plasma clearance method, respectively. Renal vascular resistance (RVR) was calculated from mean arterial pressure (MAP) and renal plasma flow.
Results Ang II decreased RPF by 34% and GFR by 9% and increased RVR by 94% and MAP by 27% (ANOVA, P < 0·001 vs. baseline, for all parameters). BQ‐123 did not alter these renal and systemic haemodynamic responses to a significant degree. In addition, BQ‐123 had no significant haemodynamic effect under baseline conditions.
Conclusions Short‐term increase of circulating Ang II levels causes systemic and renal pressor effects, which are not mitigated by endothelin ETA‐receptor blockade. This suggests that the pressor response to Ang II cannot be accounted for by the acute release of vasoactive ET‐1.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>11952807</pmid><doi>10.1046/j.1365-2362.2002.00974.x</doi><tpages>6</tpages></addata></record> |
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| subjects | Adult Angiotensin Angiotensin II - pharmacology Biological and medical sciences Cardiovascular system Cross-Over Studies Double-Blind Method endothelial function endothelial receptors Endothelin Receptor Antagonists Endothelin-1 - physiology endothelins Glomerular Filtration Rate - drug effects haemodynamics Hemodynamics - drug effects Humans Inulin Male Medical sciences Miscellaneous p-Aminohippuric Acid Peptides, Cyclic - pharmacology Pharmacology. Drug treatments Renal Circulation - drug effects Renal Plasma Flow - drug effects Vascular Resistance - drug effects |
| title | Endothelin ETA receptor-subtype specific antagonism does not mitigate the acute systemic or renal effects of exogenous angiotensin II in humans |
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