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Article: Calcium-independent phospholipase A2 plays a key role in the endothelium-dependent contractions to acetylcholine in the aorta of the spontaneously hypertensive rat

TitleCalcium-independent phospholipase A2 plays a key role in the endothelium-dependent contractions to acetylcholine in the aorta of the spontaneously hypertensive rat
Authors
Issue Date2010
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2010, v. 298 n. 4, p. H1260-H1266 How to Cite?
AbstractPhospholipase A2 (PLA2), a regulatory enzyme found in most mammalian cells, catalyzes the breakdown of membrane phospholipids to arachidonic acid. There are two major cytosolic types of the enzyme, calcium-dependent (cPLA2) and calcium-independent (iPLA2) PLA2. The present study investigated whether or not iPLA2 plays a role in the endothelium-dependent contractions of the aorta of the spontaneously hypertensive rat and its normotensive counterpart, the Wistar-Kyoto rat. The presence of iPLA2 in the endothelial cells was identified by using immunochemistry and immunoblotting. Aortic rings with and without the endothelium were suspended in organ chambers for isometric tension recording. The production of prostanoids was measured by using enzyme immunoassay kits. iPLA2 was densely distributed in endothelial cells of the aorta of both strains. At 3 x 10-6 M, the selective iPLA 2 inhibitor, bromoenol lactone (BEL), abrogated endothelium-dependent contractions induced by acetylcholine but not those evoked by the calcium ionophore A-23187. The effects of BEL were similar in the aortae of Wistar-Kyoto and spontaneously hypertensive rats. The nonselective PLA2 inhibitor quinacrine abolished the contractions triggered by both acetylcholine and A-23187, whereas the store-operated calcium channel inhibitor SKF-96365 prevented only the acetylcholine-induced contraction. The acetylcholine- but not the A-23187-induced release of 6-keto prostaglandin F1α was inhibited by BEL. The release of thromboxane B2 by either acetylcholine or A-23187 was not affected by BEL. In conclusion, iPLA 2 plays a substantial role in the generation of endothelium-derived contracting factor evoked by acetylcholine. Copyright © 2010 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/171399
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, MSKen_US
dc.contributor.authorMan, RYKen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:53Z-
dc.date.available2012-10-30T06:13:53Z-
dc.date.issued2010en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2010, v. 298 n. 4, p. H1260-H1266en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/171399-
dc.description.abstractPhospholipase A2 (PLA2), a regulatory enzyme found in most mammalian cells, catalyzes the breakdown of membrane phospholipids to arachidonic acid. There are two major cytosolic types of the enzyme, calcium-dependent (cPLA2) and calcium-independent (iPLA2) PLA2. The present study investigated whether or not iPLA2 plays a role in the endothelium-dependent contractions of the aorta of the spontaneously hypertensive rat and its normotensive counterpart, the Wistar-Kyoto rat. The presence of iPLA2 in the endothelial cells was identified by using immunochemistry and immunoblotting. Aortic rings with and without the endothelium were suspended in organ chambers for isometric tension recording. The production of prostanoids was measured by using enzyme immunoassay kits. iPLA2 was densely distributed in endothelial cells of the aorta of both strains. At 3 x 10-6 M, the selective iPLA 2 inhibitor, bromoenol lactone (BEL), abrogated endothelium-dependent contractions induced by acetylcholine but not those evoked by the calcium ionophore A-23187. The effects of BEL were similar in the aortae of Wistar-Kyoto and spontaneously hypertensive rats. The nonselective PLA2 inhibitor quinacrine abolished the contractions triggered by both acetylcholine and A-23187, whereas the store-operated calcium channel inhibitor SKF-96365 prevented only the acetylcholine-induced contraction. The acetylcholine- but not the A-23187-induced release of 6-keto prostaglandin F1α was inhibited by BEL. The release of thromboxane B2 by either acetylcholine or A-23187 was not affected by BEL. In conclusion, iPLA 2 plays a substantial role in the generation of endothelium-derived contracting factor evoked by acetylcholine. Copyright © 2010 the American Physiological Society.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Enzymologyen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEndothelium, Vascular - Enzymologyen_US
dc.subject.meshHypertension - Enzymology - Physiopathologyen_US
dc.subject.meshImidazoles - Pharmacologyen_US
dc.subject.meshIonophores - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effects - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Enzymologyen_US
dc.subject.meshNaphthalenes - Pharmacologyen_US
dc.subject.meshPhosphodiesterase Inhibitors - Pharmacologyen_US
dc.subject.meshPhospholipases A2, Calcium-Independent - Metabolismen_US
dc.subject.meshPyrones - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleCalcium-independent phospholipase A2 plays a key role in the endothelium-dependent contractions to acetylcholine in the aorta of the spontaneously hypertensive raten_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1152/ajpheart.01068.2009en_US
dc.identifier.pmid20118407-
dc.identifier.scopuseid_2-s2.0-77949760342en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77949760342&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume298en_US
dc.identifier.issue4en_US
dc.identifier.spageH1260en_US
dc.identifier.epageH1266en_US
dc.identifier.isiWOS:000275768600017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWong, MSK=23483301500en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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