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Article: Mechanisms underlying ATP-induced endothelium-dependent contractions in the SHR aorta

TitleMechanisms underlying ATP-induced endothelium-dependent contractions in the SHR aorta
Authors
KeywordsATP
Endoperoxide
Endothelium-dependent contraction
Prostacyclin
Prostanoid TP receptor
Thromboxane A 2
Issue Date2007
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2007, v. 556 n. 1-3, p. 107-114 How to Cite?
AbstractIn mature spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats, acetylcholine, the calcium ionophore A 23187 and ATP release endothelium-derived contracting factor (EDCF), cyclooxygenase (COX) derivatives that activate thromboxane-endoperoxide (TP) receptors on vascular smooth muscle. The EDCFs released by acetylcholine have been identified as prostacyclin and prostaglandin (PG) H 2 while in response to A 23187 thromboxane A 2, along with the two other prostaglandins, contributes to the endothelium-dependent contractions. The purpose of the present study was to identify the EDCFs produced by ATP. Isometric tension and the release of prostaglandins were measured in isolated aortic rings of WKY rats and SHR. ATP produced the endothelium-dependent release of prostacyclin, thromboxane A 2 and PGE 2 (PGI 2 ≫ TXA 2 ≥ PGE 2 > PGF 2α) in a similar manner in aorta from WKY rats and SHR. In SHR aortas, the release of thromboxane A 2 was significantly larger in response to ATP than to acetylcholine while that to prostacyclin was significantly smaller. The inhibition of cyclooxygenase with indomethacin prevented the release of prostaglandins and the occurrence of endothelium-dependent contractions. The thromboxane synthase inhibitor dazoxiben selectively abolished the ATP-dependent production of thromboxane A 2 and partially inhibited the corresponding endothelium-dependent contractions. U 51605, a non-selective inhibitor of PGI-synthase, reduced the release of prostacyclin elicited by ATP but induced a parallel increase in the production of PGE 2 and PGF 2α, suggestive of a PGH 2-spillover, which was associated with the enhancement of the endothelium-dependent contractions. Thus, in the aorta of SHR, endothelium-dependent contractions elicited by ATP involve the release of thromboxane A 2 and prostacyclin with a possible contribution of PGH 2. © 2006 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/80186
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGluais, Pen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorFélétou, Men_HK
dc.date.accessioned2010-09-06T08:03:27Z-
dc.date.available2010-09-06T08:03:27Z-
dc.date.issued2007en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2007, v. 556 n. 1-3, p. 107-114en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80186-
dc.description.abstractIn mature spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats, acetylcholine, the calcium ionophore A 23187 and ATP release endothelium-derived contracting factor (EDCF), cyclooxygenase (COX) derivatives that activate thromboxane-endoperoxide (TP) receptors on vascular smooth muscle. The EDCFs released by acetylcholine have been identified as prostacyclin and prostaglandin (PG) H 2 while in response to A 23187 thromboxane A 2, along with the two other prostaglandins, contributes to the endothelium-dependent contractions. The purpose of the present study was to identify the EDCFs produced by ATP. Isometric tension and the release of prostaglandins were measured in isolated aortic rings of WKY rats and SHR. ATP produced the endothelium-dependent release of prostacyclin, thromboxane A 2 and PGE 2 (PGI 2 ≫ TXA 2 ≥ PGE 2 > PGF 2α) in a similar manner in aorta from WKY rats and SHR. In SHR aortas, the release of thromboxane A 2 was significantly larger in response to ATP than to acetylcholine while that to prostacyclin was significantly smaller. The inhibition of cyclooxygenase with indomethacin prevented the release of prostaglandins and the occurrence of endothelium-dependent contractions. The thromboxane synthase inhibitor dazoxiben selectively abolished the ATP-dependent production of thromboxane A 2 and partially inhibited the corresponding endothelium-dependent contractions. U 51605, a non-selective inhibitor of PGI-synthase, reduced the release of prostacyclin elicited by ATP but induced a parallel increase in the production of PGE 2 and PGF 2α, suggestive of a PGH 2-spillover, which was associated with the enhancement of the endothelium-dependent contractions. Thus, in the aorta of SHR, endothelium-dependent contractions elicited by ATP involve the release of thromboxane A 2 and prostacyclin with a possible contribution of PGH 2. © 2006 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.rightsEuropean Journal of Pharmacology . Copyright © Elsevier BV.en_HK
dc.subjectATPen_HK
dc.subjectEndoperoxideen_HK
dc.subjectEndothelium-dependent contractionen_HK
dc.subjectProstacyclinen_HK
dc.subjectProstanoid TP receptoren_HK
dc.subjectThromboxane A 2en_HK
dc.titleMechanisms underlying ATP-induced endothelium-dependent contractions in the SHR aortaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2999&volume=556&spage=107&epage=114&date=2006&atitle=Mechanisms+underlying+ATP-induced+endothelium-dependent+contractions+in+the+SHR+aortaen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ejphar.2006.10.050en_HK
dc.identifier.pmid17126320-
dc.identifier.scopuseid_2-s2.0-33846067638en_HK
dc.identifier.hkuros136325en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846067638&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume556en_HK
dc.identifier.issue1-3en_HK
dc.identifier.spage107en_HK
dc.identifier.epage114en_HK
dc.identifier.isiWOS:000244580100016-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridGluais, P=6602456462en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK

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