Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types
1 Department of Physiology and Cell Biology and 2 Davis Heart and Lung Research Institute, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 43210 Submitted 9 December 2003 ; accepted in final form 7 April 2004 Mice have been increasingly used as models for investigati...
Gespeichert in:
| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2004-08, Vol.287 (2), p.H573-H578 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | H578 |
|---|---|
| container_issue | 2 |
| container_start_page | H573 |
| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 287 |
| creator | Zhou, Yingbi Dirksen, Wessel P Zweier, Jay L Periasamy, Muthu |
| description | 1 Department of Physiology and Cell Biology and 2 Davis Heart and Lung Research Institute, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 43210
Submitted 9 December 2003
; accepted in final form 7 April 2004
Mice have been increasingly used as models for investigating cardiovascular diseases. However, the responsiveness of mouse vasculature to endothelin (ET)-1 has not been clearly established. The goal of this study was to determine the role of ET receptors (ET A and ET B ) in mouse vessels using isometric force measurements. Results showed that in the abdominal aorta ET-1 induced a concentration-dependent contraction (EC 50 : 1.4 nM) with maximum reaching 89.5 ± 4.9% (10 nM) of that induced by 60 mM K + [with nitric oxide synthase (NOS) inhibitor N -nitro- L -arginine methyl ester ( L -NAME)]. However, in the thoracic aorta or the carotid artery, ET-1 was poorly effective. RT-PCR revealed that in the endothelium-denuded abdominal aorta, the PCR product for ET B receptors was very low compared with ET A . Similarly in tissues treated with L -NAME, the ET B receptor-specific agonist sarafotoxin 6c (S6c; 100 nM) induced only a minimal contraction ( |
| doi_str_mv | 10.1152/ajpheart.01170.2003 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1152_ajpheart_01170_2003</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>66748990</sourcerecordid><originalsourceid>FETCH-LOGICAL-c457t-10c42e27b9daad038d60b4fb07d98ecc51b90f91581b36adef8d0144094124dc3</originalsourceid><addsrcrecordid>eNp1kE1v3CAQhlHVqNmm_QWVKk69eTOA8UduVZSPSpFySc8Iw3jtiAUX7Db778Nmt8kppxHD-7waPYR8Y7BmTPJz_TgNqOO8BsZqWHMA8YGs8g8vmBTtR7ICUYmiYkKeks8pPQKArCvxiZwyCTVvK7YimytvwzygG33BitHbxaClEdMUfMJER0_HFJye83YbloT0L6aELl3QTFF8mnI2jcFT7S3tF2_m_SP0ucPgNIdI592E6Qs56bVL-PU4z8jv66uHy9vi7v7m1-XPu8KUsp4LBqbkyOuutVpbEI2toCv7DmrbNmiMZF0LfctkwzpRaYt9Y4GVJbQl46U14oz8OPROMfxZMM1qOyaDzmmP-XxVVXXZtC3koDgETQwpRezVFMetjjvFQO39qv9-1Ytftfebqe_H-qXbon1jjkJz4OIQGMbN8G-MqKZhl_24sNmp68W5B3yaX6t5UyuubmUt1GT7DK_fh1_PeYPEMwmkoIY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>66748990</pqid></control><display><type>article</type><title>Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types</title><source>MEDLINE</source><source>American Physiological Society</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Zhou, Yingbi ; Dirksen, Wessel P ; Zweier, Jay L ; Periasamy, Muthu</creator><creatorcontrib>Zhou, Yingbi ; Dirksen, Wessel P ; Zweier, Jay L ; Periasamy, Muthu</creatorcontrib><description>1 Department of Physiology and Cell Biology and 2 Davis Heart and Lung Research Institute, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 43210
Submitted 9 December 2003
; accepted in final form 7 April 2004
Mice have been increasingly used as models for investigating cardiovascular diseases. However, the responsiveness of mouse vasculature to endothelin (ET)-1 has not been clearly established. The goal of this study was to determine the role of ET receptors (ET A and ET B ) in mouse vessels using isometric force measurements. Results showed that in the abdominal aorta ET-1 induced a concentration-dependent contraction (EC 50 : 1.4 nM) with maximum reaching 89.5 ± 4.9% (10 nM) of that induced by 60 mM K + [with nitric oxide synthase (NOS) inhibitor N -nitro- L -arginine methyl ester ( L -NAME)]. However, in the thoracic aorta or the carotid artery, ET-1 was poorly effective. RT-PCR revealed that in the endothelium-denuded abdominal aorta, the PCR product for ET B receptors was very low compared with ET A . Similarly in tissues treated with L -NAME, the ET B receptor-specific agonist sarafotoxin 6c (S6c; 100 nM) induced only a minimal contraction (<5%). Meanwhile, the ET A antagonist BQ-123 (1 µM) completely inhibited the maximum ET-1 (10 nM) contractile response. Furthermore, we found that in the abdominal aorta that had not been treated with L -NAME, ET-1-induced contraction significantly decreased. However, in such specimens, S6c was unable to induce any relaxation on phenylephrine-induced contraction. These results indicate that the role of ET receptors differs considerably among mouse vessels. In the abdominal aorta, ET A receptor mediates a potent vasoconstrictor response, whereas ET B has, if any, only a minimal functional presence. Also, our data suggest that ET-1 might involve a NOS-dependent vasodilation in the abdominal aorta, which remains to be further defined.
endothelin A receptor; endothelin B receptor; vasoconstriction; nitric oxide synthase; vasodilation
Address for reprint requests and other correspondence: M. Periasamy, Dept. of Physiology and Cell Biology, The Ohio State Univ. College of Medicine, 304 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210 (E-mail: periasamy.1{at}osu.edu ).</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.01170.2003</identifier><identifier>PMID: 15072961</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Aorta, Abdominal - drug effects ; Aorta, Abdominal - metabolism ; Aorta, Abdominal - physiology ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - metabolism ; Aorta, Thoracic - physiology ; Carotid Arteries - drug effects ; Carotid Arteries - metabolism ; Carotid Arteries - physiology ; Endothelin A Receptor Antagonists ; Endothelin-1 - pharmacology ; In Vitro Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Nitric Oxide Synthase - metabolism ; Peptides, Cyclic - pharmacology ; Receptor, Endothelin A - genetics ; Receptor, Endothelin B - agonists ; Receptor, Endothelin B - genetics ; RNA, Messenger - metabolism ; Vasoconstriction - drug effects ; Vasoconstrictor Agents - pharmacology ; Viper Venoms - pharmacology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2004-08, Vol.287 (2), p.H573-H578</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-10c42e27b9daad038d60b4fb07d98ecc51b90f91581b36adef8d0144094124dc3</citedby><cites>FETCH-LOGICAL-c457t-10c42e27b9daad038d60b4fb07d98ecc51b90f91581b36adef8d0144094124dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,3028,27911,27912</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15072961$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Yingbi</creatorcontrib><creatorcontrib>Dirksen, Wessel P</creatorcontrib><creatorcontrib>Zweier, Jay L</creatorcontrib><creatorcontrib>Periasamy, Muthu</creatorcontrib><title>Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>1 Department of Physiology and Cell Biology and 2 Davis Heart and Lung Research Institute, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 43210
Submitted 9 December 2003
; accepted in final form 7 April 2004
Mice have been increasingly used as models for investigating cardiovascular diseases. However, the responsiveness of mouse vasculature to endothelin (ET)-1 has not been clearly established. The goal of this study was to determine the role of ET receptors (ET A and ET B ) in mouse vessels using isometric force measurements. Results showed that in the abdominal aorta ET-1 induced a concentration-dependent contraction (EC 50 : 1.4 nM) with maximum reaching 89.5 ± 4.9% (10 nM) of that induced by 60 mM K + [with nitric oxide synthase (NOS) inhibitor N -nitro- L -arginine methyl ester ( L -NAME)]. However, in the thoracic aorta or the carotid artery, ET-1 was poorly effective. RT-PCR revealed that in the endothelium-denuded abdominal aorta, the PCR product for ET B receptors was very low compared with ET A . Similarly in tissues treated with L -NAME, the ET B receptor-specific agonist sarafotoxin 6c (S6c; 100 nM) induced only a minimal contraction (<5%). Meanwhile, the ET A antagonist BQ-123 (1 µM) completely inhibited the maximum ET-1 (10 nM) contractile response. Furthermore, we found that in the abdominal aorta that had not been treated with L -NAME, ET-1-induced contraction significantly decreased. However, in such specimens, S6c was unable to induce any relaxation on phenylephrine-induced contraction. These results indicate that the role of ET receptors differs considerably among mouse vessels. In the abdominal aorta, ET A receptor mediates a potent vasoconstrictor response, whereas ET B has, if any, only a minimal functional presence. Also, our data suggest that ET-1 might involve a NOS-dependent vasodilation in the abdominal aorta, which remains to be further defined.
endothelin A receptor; endothelin B receptor; vasoconstriction; nitric oxide synthase; vasodilation
Address for reprint requests and other correspondence: M. Periasamy, Dept. of Physiology and Cell Biology, The Ohio State Univ. College of Medicine, 304 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210 (E-mail: periasamy.1{at}osu.edu ).</description><subject>Animals</subject><subject>Aorta, Abdominal - drug effects</subject><subject>Aorta, Abdominal - metabolism</subject><subject>Aorta, Abdominal - physiology</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - metabolism</subject><subject>Aorta, Thoracic - physiology</subject><subject>Carotid Arteries - drug effects</subject><subject>Carotid Arteries - metabolism</subject><subject>Carotid Arteries - physiology</subject><subject>Endothelin A Receptor Antagonists</subject><subject>Endothelin-1 - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Peptides, Cyclic - pharmacology</subject><subject>Receptor, Endothelin A - genetics</subject><subject>Receptor, Endothelin B - agonists</subject><subject>Receptor, Endothelin B - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Viper Venoms - pharmacology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1v3CAQhlHVqNmm_QWVKk69eTOA8UduVZSPSpFySc8Iw3jtiAUX7Db778Nmt8kppxHD-7waPYR8Y7BmTPJz_TgNqOO8BsZqWHMA8YGs8g8vmBTtR7ICUYmiYkKeks8pPQKArCvxiZwyCTVvK7YimytvwzygG33BitHbxaClEdMUfMJER0_HFJye83YbloT0L6aELl3QTFF8mnI2jcFT7S3tF2_m_SP0ucPgNIdI592E6Qs56bVL-PU4z8jv66uHy9vi7v7m1-XPu8KUsp4LBqbkyOuutVpbEI2toCv7DmrbNmiMZF0LfctkwzpRaYt9Y4GVJbQl46U14oz8OPROMfxZMM1qOyaDzmmP-XxVVXXZtC3koDgETQwpRezVFMetjjvFQO39qv9-1Ytftfebqe_H-qXbon1jjkJz4OIQGMbN8G-MqKZhl_24sNmp68W5B3yaX6t5UyuubmUt1GT7DK_fh1_PeYPEMwmkoIY</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>Zhou, Yingbi</creator><creator>Dirksen, Wessel P</creator><creator>Zweier, Jay L</creator><creator>Periasamy, Muthu</creator><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>20040801</creationdate><title>Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types</title><author>Zhou, Yingbi ; Dirksen, Wessel P ; Zweier, Jay L ; Periasamy, Muthu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-10c42e27b9daad038d60b4fb07d98ecc51b90f91581b36adef8d0144094124dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Aorta, Abdominal - drug effects</topic><topic>Aorta, Abdominal - metabolism</topic><topic>Aorta, Abdominal - physiology</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - metabolism</topic><topic>Aorta, Thoracic - physiology</topic><topic>Carotid Arteries - drug effects</topic><topic>Carotid Arteries - metabolism</topic><topic>Carotid Arteries - physiology</topic><topic>Endothelin A Receptor Antagonists</topic><topic>Endothelin-1 - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Peptides, Cyclic - pharmacology</topic><topic>Receptor, Endothelin A - genetics</topic><topic>Receptor, Endothelin B - agonists</topic><topic>Receptor, Endothelin B - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Viper Venoms - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Yingbi</creatorcontrib><creatorcontrib>Dirksen, Wessel P</creatorcontrib><creatorcontrib>Zweier, Jay L</creatorcontrib><creatorcontrib>Periasamy, Muthu</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>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Yingbi</au><au>Dirksen, Wessel P</au><au>Zweier, Jay L</au><au>Periasamy, Muthu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>287</volume><issue>2</issue><spage>H573</spage><epage>H578</epage><pages>H573-H578</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>1 Department of Physiology and Cell Biology and 2 Davis Heart and Lung Research Institute, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 43210
Submitted 9 December 2003
; accepted in final form 7 April 2004
Mice have been increasingly used as models for investigating cardiovascular diseases. However, the responsiveness of mouse vasculature to endothelin (ET)-1 has not been clearly established. The goal of this study was to determine the role of ET receptors (ET A and ET B ) in mouse vessels using isometric force measurements. Results showed that in the abdominal aorta ET-1 induced a concentration-dependent contraction (EC 50 : 1.4 nM) with maximum reaching 89.5 ± 4.9% (10 nM) of that induced by 60 mM K + [with nitric oxide synthase (NOS) inhibitor N -nitro- L -arginine methyl ester ( L -NAME)]. However, in the thoracic aorta or the carotid artery, ET-1 was poorly effective. RT-PCR revealed that in the endothelium-denuded abdominal aorta, the PCR product for ET B receptors was very low compared with ET A . Similarly in tissues treated with L -NAME, the ET B receptor-specific agonist sarafotoxin 6c (S6c; 100 nM) induced only a minimal contraction (<5%). Meanwhile, the ET A antagonist BQ-123 (1 µM) completely inhibited the maximum ET-1 (10 nM) contractile response. Furthermore, we found that in the abdominal aorta that had not been treated with L -NAME, ET-1-induced contraction significantly decreased. However, in such specimens, S6c was unable to induce any relaxation on phenylephrine-induced contraction. These results indicate that the role of ET receptors differs considerably among mouse vessels. In the abdominal aorta, ET A receptor mediates a potent vasoconstrictor response, whereas ET B has, if any, only a minimal functional presence. Also, our data suggest that ET-1 might involve a NOS-dependent vasodilation in the abdominal aorta, which remains to be further defined.
endothelin A receptor; endothelin B receptor; vasoconstriction; nitric oxide synthase; vasodilation
Address for reprint requests and other correspondence: M. Periasamy, Dept. of Physiology and Cell Biology, The Ohio State Univ. College of Medicine, 304 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210 (E-mail: periasamy.1{at}osu.edu ).</abstract><cop>United States</cop><pmid>15072961</pmid><doi>10.1152/ajpheart.01170.2003</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2004-08, Vol.287 (2), p.H573-H578 |
| issn | 0363-6135 1522-1539 |
| language | eng |
| recordid | cdi_crossref_primary_10_1152_ajpheart_01170_2003 |
| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Aorta, Abdominal - drug effects Aorta, Abdominal - metabolism Aorta, Abdominal - physiology Aorta, Thoracic - drug effects Aorta, Thoracic - metabolism Aorta, Thoracic - physiology Carotid Arteries - drug effects Carotid Arteries - metabolism Carotid Arteries - physiology Endothelin A Receptor Antagonists Endothelin-1 - pharmacology In Vitro Techniques Male Mice Mice, Inbred C57BL Nitric Oxide Synthase - metabolism Peptides, Cyclic - pharmacology Receptor, Endothelin A - genetics Receptor, Endothelin B - agonists Receptor, Endothelin B - genetics RNA, Messenger - metabolism Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology Viper Venoms - pharmacology |
| title | Endothelin-1-induced responses in isolated mouse vessels: the expression and function of receptor types |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-15T17%3A37%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Endothelin-1-induced%20responses%20in%20isolated%20mouse%20vessels:%20the%20expression%20and%20function%20of%20receptor%20types&rft.jtitle=American%20journal%20of%20physiology.%20Heart%20and%20circulatory%20physiology&rft.au=Zhou,%20Yingbi&rft.date=2004-08-01&rft.volume=287&rft.issue=2&rft.spage=H573&rft.epage=H578&rft.pages=H573-H578&rft.issn=0363-6135&rft.eissn=1522-1539&rft_id=info:doi/10.1152/ajpheart.01170.2003&rft_dat=%3Cproquest_cross%3E66748990%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=66748990&rft_id=info:pmid/15072961&rfr_iscdi=true |