Rationale and Perspective of Endothelin-1 Antagonism in Acute Heart Failure
A role of the potent and long-acting vasoconstrictor peptide endothelin (ET)-1 in the pathophysiology of chronic human heart failure has been postulated, based upon indirect evidence such as elevated plasma ET-1 levels and their relationship to the degree of haemodynamic impairment. Acute heart fail...
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Veröffentlicht in: | Journal of cardiovascular pharmacology 2001-11, Vol.38 Suppl 2, p.S53-S57 |
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container_title | Journal of cardiovascular pharmacology |
container_volume | 38 Suppl 2 |
creator | Kiowski, Wolfgang Suetsch, Gabor Oechslin, Erwin Schalcher, Christoph Brunner-LaRocca, Hans P Bertel, Osmund |
description | A role of the potent and long-acting vasoconstrictor peptide endothelin (ET)-1 in the pathophysiology of chronic human heart failure has been postulated, based upon indirect evidence such as elevated plasma ET-1 levels and their relationship to the degree of haemodynamic impairment. Acute heart failure shares many features of chronic heart failure, albeit in an exaggerated fashion. As both the mixed ETA/ETB-receptor antagonist bosentan and the selective ETA receptor antagonist BQ 123 acutely improved the haemodynamics of chronic heart failure patients, there seems to be good reason to believe that ET-1 receptor antagonism may also be of benefit in the setting of acute heart failure. However, appropriate trials will have to be performed to document the clinical benefit of such an approach. Finally, the question remains open as to whether mixed ET-1 receptor antagonists like bosentan will prove better, worse or equal to antagonists that block the ETA receptor only. |
doi_str_mv | 10.1097/00005344-200111002-00014 |
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Acute heart failure shares many features of chronic heart failure, albeit in an exaggerated fashion. As both the mixed ETA/ETB-receptor antagonist bosentan and the selective ETA receptor antagonist BQ 123 acutely improved the haemodynamics of chronic heart failure patients, there seems to be good reason to believe that ET-1 receptor antagonism may also be of benefit in the setting of acute heart failure. However, appropriate trials will have to be performed to document the clinical benefit of such an approach. Finally, the question remains open as to whether mixed ET-1 receptor antagonists like bosentan will prove better, worse or equal to antagonists that block the ETA receptor only.</description><identifier>ISSN: 0160-2446</identifier><identifier>EISSN: 1533-4023</identifier><identifier>DOI: 10.1097/00005344-200111002-00014</identifier><identifier>PMID: 11811379</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins, Inc</publisher><subject>Acute Disease ; Animals ; Antihypertensive Agents - therapeutic use ; Bosentan ; Dogs ; Endothelin Receptor Antagonists ; Endothelin-1 - antagonists & inhibitors ; Endothelin-1 - blood ; Heart Failure - drug therapy ; Heart Failure - physiopathology ; Humans ; Peptides, Cyclic - therapeutic use ; Receptor, Endothelin A ; Receptor, Endothelin B ; Sulfonamides - therapeutic use</subject><ispartof>Journal of cardiovascular pharmacology, 2001-11, Vol.38 Suppl 2, p.S53-S57</ispartof><rights>2001 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4724-6b19ffdb9a88c556a32ba4be2adad612f0325ad9f07ca3ac3d17944234bc19fb3</citedby><cites>FETCH-LOGICAL-c4724-6b19ffdb9a88c556a32ba4be2adad612f0325ad9f07ca3ac3d17944234bc19fb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00005344-200111002-00014$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>314,776,780,4595,27901,27902,65206</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11811379$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kiowski, Wolfgang</creatorcontrib><creatorcontrib>Suetsch, Gabor</creatorcontrib><creatorcontrib>Oechslin, Erwin</creatorcontrib><creatorcontrib>Schalcher, Christoph</creatorcontrib><creatorcontrib>Brunner-LaRocca, Hans P</creatorcontrib><creatorcontrib>Bertel, Osmund</creatorcontrib><title>Rationale and Perspective of Endothelin-1 Antagonism in Acute Heart Failure</title><title>Journal of cardiovascular pharmacology</title><addtitle>J Cardiovasc Pharmacol</addtitle><description>A role of the potent and long-acting vasoconstrictor peptide endothelin (ET)-1 in the pathophysiology of chronic human heart failure has been postulated, based upon indirect evidence such as elevated plasma ET-1 levels and their relationship to the degree of haemodynamic impairment. Acute heart failure shares many features of chronic heart failure, albeit in an exaggerated fashion. As both the mixed ETA/ETB-receptor antagonist bosentan and the selective ETA receptor antagonist BQ 123 acutely improved the haemodynamics of chronic heart failure patients, there seems to be good reason to believe that ET-1 receptor antagonism may also be of benefit in the setting of acute heart failure. However, appropriate trials will have to be performed to document the clinical benefit of such an approach. Finally, the question remains open as to whether mixed ET-1 receptor antagonists like bosentan will prove better, worse or equal to antagonists that block the ETA receptor only.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Bosentan</subject><subject>Dogs</subject><subject>Endothelin Receptor Antagonists</subject><subject>Endothelin-1 - antagonists & inhibitors</subject><subject>Endothelin-1 - blood</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - physiopathology</subject><subject>Humans</subject><subject>Peptides, Cyclic - therapeutic use</subject><subject>Receptor, Endothelin A</subject><subject>Receptor, Endothelin B</subject><subject>Sulfonamides - therapeutic use</subject><issn>0160-2446</issn><issn>1533-4023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFOwzAMhiMEgjF4BZQTt0KcpO16nKYNEEggBOfITV1WyNqRpCDensIGnPDFkvX9tvSZMQ7iDESRn4uhUqV1IoUAACFkMkxA77ARpEolWki1y0YCMpFIrbMDdhjC8xeR5tk-OwCYAKi8GLHre4xN16Ijjm3F78iHNdnYvBHvaj5vqy4uyTVtAnzaRnzq2iaseNPyqe0j8UtCH_kCG9d7OmJ7NbpAx9s-Zo-L-cPsMrm5vbiaTW8Sq3Opk6yEoq6rssDJxKZphkqWqEuSWGGVgayFkilWRS1yiwqtqiAvtJZKl3ZIlmrMTjd717577SlEs2qCJeewpa4PZjgCCoQewMkGtL4LwVNt1r5Zof8wIMyXSPMj0vyKNN8ih-jJ9kZfrqj6C27NDYDeAO-di4O1F9e_kzdLQheX5r8HqU8ir3z-</recordid><startdate>200111</startdate><enddate>200111</enddate><creator>Kiowski, Wolfgang</creator><creator>Suetsch, Gabor</creator><creator>Oechslin, Erwin</creator><creator>Schalcher, Christoph</creator><creator>Brunner-LaRocca, Hans P</creator><creator>Bertel, Osmund</creator><general>Lippincott Williams & Wilkins, Inc</general><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>200111</creationdate><title>Rationale and Perspective of Endothelin-1 Antagonism in Acute Heart Failure</title><author>Kiowski, Wolfgang ; Suetsch, Gabor ; Oechslin, Erwin ; Schalcher, Christoph ; Brunner-LaRocca, Hans P ; Bertel, Osmund</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4724-6b19ffdb9a88c556a32ba4be2adad612f0325ad9f07ca3ac3d17944234bc19fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Bosentan</topic><topic>Dogs</topic><topic>Endothelin Receptor Antagonists</topic><topic>Endothelin-1 - antagonists & inhibitors</topic><topic>Endothelin-1 - blood</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - physiopathology</topic><topic>Humans</topic><topic>Peptides, Cyclic - therapeutic use</topic><topic>Receptor, Endothelin A</topic><topic>Receptor, Endothelin B</topic><topic>Sulfonamides - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kiowski, Wolfgang</creatorcontrib><creatorcontrib>Suetsch, Gabor</creatorcontrib><creatorcontrib>Oechslin, Erwin</creatorcontrib><creatorcontrib>Schalcher, Christoph</creatorcontrib><creatorcontrib>Brunner-LaRocca, Hans P</creatorcontrib><creatorcontrib>Bertel, Osmund</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>Journal of cardiovascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kiowski, Wolfgang</au><au>Suetsch, Gabor</au><au>Oechslin, Erwin</au><au>Schalcher, Christoph</au><au>Brunner-LaRocca, Hans P</au><au>Bertel, Osmund</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rationale and Perspective of Endothelin-1 Antagonism in Acute Heart Failure</atitle><jtitle>Journal of cardiovascular pharmacology</jtitle><addtitle>J Cardiovasc Pharmacol</addtitle><date>2001-11</date><risdate>2001</risdate><volume>38 Suppl 2</volume><spage>S53</spage><epage>S57</epage><pages>S53-S57</pages><issn>0160-2446</issn><eissn>1533-4023</eissn><abstract>A role of the potent and long-acting vasoconstrictor peptide endothelin (ET)-1 in the pathophysiology of chronic human heart failure has been postulated, based upon indirect evidence such as elevated plasma ET-1 levels and their relationship to the degree of haemodynamic impairment. Acute heart failure shares many features of chronic heart failure, albeit in an exaggerated fashion. As both the mixed ETA/ETB-receptor antagonist bosentan and the selective ETA receptor antagonist BQ 123 acutely improved the haemodynamics of chronic heart failure patients, there seems to be good reason to believe that ET-1 receptor antagonism may also be of benefit in the setting of acute heart failure. However, appropriate trials will have to be performed to document the clinical benefit of such an approach. Finally, the question remains open as to whether mixed ET-1 receptor antagonists like bosentan will prove better, worse or equal to antagonists that block the ETA receptor only.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>11811379</pmid><doi>10.1097/00005344-200111002-00014</doi><oa>free_for_read</oa></addata></record> |
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source | Journals@Ovid Ovid Autoload; MEDLINE; Journals@Ovid LWW Legacy Archive; EZB-FREE-00999 freely available EZB journals |
subjects | Acute Disease Animals Antihypertensive Agents - therapeutic use Bosentan Dogs Endothelin Receptor Antagonists Endothelin-1 - antagonists & inhibitors Endothelin-1 - blood Heart Failure - drug therapy Heart Failure - physiopathology Humans Peptides, Cyclic - therapeutic use Receptor, Endothelin A Receptor, Endothelin B Sulfonamides - therapeutic use |
title | Rationale and Perspective of Endothelin-1 Antagonism in Acute Heart Failure |
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