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Article: Endothelin-1 and -3 cause endothelium-dependent hyperpolarization in the rat mesenteric artery
Title | Endothelin-1 and -3 cause endothelium-dependent hyperpolarization in the rat mesenteric artery |
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Authors | |
Keywords | BQ-123 endothelin(B) receptor endothelium-derived hyperpolarizing factor endothelium-derived relaxing factor IRL-1620 spontaneously hypertensive rats Wistar-Kyoto rats |
Issue Date | 1993 |
Publisher | American Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/ |
Citation | American Journal Of Physiology - Heart And Circulatory Physiology, 1993, v. 265 n. 6 34-6, p. H2137-H2141 How to Cite? |
Abstract | The present study was designed to determine whether endothelin (ET) induces endothelium-dependent hyperpolarization in the isolated rat mesenteric artery and, if so, to identify the receptor subtype involved. Main superior mesenteric arteries of Wistar-Kyoto and spontaneously hypertensive rats were used for the measurement of electrical responses of smooth muscle cells, using glass microelectrode. In tissues with endothelium of both strains, ET-1 (10-8 M) caused an initial transient hyperpolarization followed by a sustained depolarization. In tissues without endothelium, only depolarization was observed. ET-3 (10-8 M) produced transient hyperpolarizations only in preparations with endothelium. There was no significant difference in maximal amplitude of hyperpolarization between the two strains. BQ-123 (selective ET(A)-receptor antagonist) blocked the depolarization to ET-1 but did not inhibit hyperpolarizing responses to either isopeptide. IRL-1620 (specific ET(B)-receptor agonist) produced transient membrane hyperpolarizations in tissues with endothelium. The hyperpolarizations induced by ET were not affected by N(G)-nitro-L-arginine. These data suggest that both ET-1 and ET-3 can cause endothelium-dependent hyperpolarization in the rat mesenteric artery and that the endothelial receptor involved may belong to ET(B) subtype. |
Persistent Identifier | http://hdl.handle.net/10722/171081 |
ISSN |
DC Field | Value | Language |
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dc.contributor.author | Nakashima, M | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:12:07Z | - |
dc.date.available | 2012-10-30T06:12:07Z | - |
dc.date.issued | 1993 | en_US |
dc.identifier.citation | American Journal Of Physiology - Heart And Circulatory Physiology, 1993, v. 265 n. 6 34-6, p. H2137-H2141 | en_US |
dc.identifier.issn | 0002-9513 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171081 | - |
dc.description.abstract | The present study was designed to determine whether endothelin (ET) induces endothelium-dependent hyperpolarization in the isolated rat mesenteric artery and, if so, to identify the receptor subtype involved. Main superior mesenteric arteries of Wistar-Kyoto and spontaneously hypertensive rats were used for the measurement of electrical responses of smooth muscle cells, using glass microelectrode. In tissues with endothelium of both strains, ET-1 (10-8 M) caused an initial transient hyperpolarization followed by a sustained depolarization. In tissues without endothelium, only depolarization was observed. ET-3 (10-8 M) produced transient hyperpolarizations only in preparations with endothelium. There was no significant difference in maximal amplitude of hyperpolarization between the two strains. BQ-123 (selective ET(A)-receptor antagonist) blocked the depolarization to ET-1 but did not inhibit hyperpolarizing responses to either isopeptide. IRL-1620 (specific ET(B)-receptor agonist) produced transient membrane hyperpolarizations in tissues with endothelium. The hyperpolarizations induced by ET were not affected by N(G)-nitro-L-arginine. These data suggest that both ET-1 and ET-3 can cause endothelium-dependent hyperpolarization in the rat mesenteric artery and that the endothelial receptor involved may belong to ET(B) subtype. | en_US |
dc.language | eng | en_US |
dc.publisher | American Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/ | en_US |
dc.relation.ispartof | American Journal of Physiology - Heart and Circulatory Physiology | en_US |
dc.subject | BQ-123 | - |
dc.subject | endothelin(B) receptor | - |
dc.subject | endothelium-derived hyperpolarizing factor | - |
dc.subject | endothelium-derived relaxing factor | - |
dc.subject | IRL-1620 | - |
dc.subject | spontaneously hypertensive rats | - |
dc.subject | Wistar-Kyoto rats | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Biological Factors - Metabolism | en_US |
dc.subject.mesh | Electrophysiology | en_US |
dc.subject.mesh | Endothelins - Pharmacology | en_US |
dc.subject.mesh | Endothelium, Vascular - Drug Effects - Metabolism - Physiology | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Mesenteric Arteries - Drug Effects - Metabolism - Physiology | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Rats, Inbred Shr | en_US |
dc.subject.mesh | Rats, Inbred Wky | en_US |
dc.subject.mesh | Receptors, Endothelin - Physiology | en_US |
dc.title | Endothelin-1 and -3 cause endothelium-dependent hyperpolarization in the rat mesenteric artery | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 8285253 | - |
dc.identifier.scopus | eid_2-s2.0-0027132737 | en_US |
dc.identifier.volume | 265 | en_US |
dc.identifier.issue | 6 34-6 | en_US |
dc.identifier.spage | H2137 | en_US |
dc.identifier.epage | H2141 | en_US |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Nakashima, M=35599797500 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0002-9513 | - |