File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Effect of ryanodine in dog mesenteric artery: Interference with potassium and adrenergic stimulation

TitleEffect of ryanodine in dog mesenteric artery: Interference with potassium and adrenergic stimulation
Authors
Issue Date1991
Citation
Journal Of Vascular Medicine And Biology, 1991, v. 3 n. 4, p. 167-173 How to Cite?
AbstractRyanodine, a selective pharmacological tool affecting sarcoplasmic reticulum Ca2+-release channels in skeletal and cardiac muscles, was tested on contractions induced in the dog mesenteric artery by high-KCl depolarization and α-adrenergic stimulation. Ryanodine significantly potentiated tonic contractions induced by low-KCl (25-45 mM) and norepinephrine (30 nM-3 μM) stimulations. KCl potentiation was only partly sensitive to nifedipine and norepinephrine potentiation to prazosin. Tonic contractions produced by stimulation with higher KCl and norepinephrine concentrations were not potentiated, but rather attenuated, by ryanodine. In Ca2+-free medium containing 100 μM EGTA, norepinephrine induced a dose-dependent transient contraction, which was decreased or abolished by ryanodine. When repeated in Ca2+-free solutions, norepinephrine-induced transient contractions rapidly decreased in amplitude and disappeared within four consecutive stimulations. Ryanodine accelerated the rate of decay of these serial norepinephrine stimulations. These results are consistent with the interpretation that ryanodine impairs the buffering capacity of internal Ca2+ sinks, probably by making the sarcoplasmic reticulum permeable to Ca2+.
Persistent Identifierhttp://hdl.handle.net/10722/173435
ISSN

 

DC FieldValueLanguage
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorKwan, CYen_US
dc.contributor.authorDaniel, EEen_US
dc.date.accessioned2012-10-30T06:31:24Z-
dc.date.available2012-10-30T06:31:24Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Vascular Medicine And Biology, 1991, v. 3 n. 4, p. 167-173en_US
dc.identifier.issn1042-5268en_US
dc.identifier.urihttp://hdl.handle.net/10722/173435-
dc.description.abstractRyanodine, a selective pharmacological tool affecting sarcoplasmic reticulum Ca2+-release channels in skeletal and cardiac muscles, was tested on contractions induced in the dog mesenteric artery by high-KCl depolarization and α-adrenergic stimulation. Ryanodine significantly potentiated tonic contractions induced by low-KCl (25-45 mM) and norepinephrine (30 nM-3 μM) stimulations. KCl potentiation was only partly sensitive to nifedipine and norepinephrine potentiation to prazosin. Tonic contractions produced by stimulation with higher KCl and norepinephrine concentrations were not potentiated, but rather attenuated, by ryanodine. In Ca2+-free medium containing 100 μM EGTA, norepinephrine induced a dose-dependent transient contraction, which was decreased or abolished by ryanodine. When repeated in Ca2+-free solutions, norepinephrine-induced transient contractions rapidly decreased in amplitude and disappeared within four consecutive stimulations. Ryanodine accelerated the rate of decay of these serial norepinephrine stimulations. These results are consistent with the interpretation that ryanodine impairs the buffering capacity of internal Ca2+ sinks, probably by making the sarcoplasmic reticulum permeable to Ca2+.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Vascular Medicine and Biologyen_US
dc.titleEffect of ryanodine in dog mesenteric artery: Interference with potassium and adrenergic stimulationen_US
dc.typeConference_Paperen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-0026382729en_US
dc.identifier.volume3en_US
dc.identifier.issue4en_US
dc.identifier.spage167en_US
dc.identifier.epage173en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridKwan, CY=7201421224en_US
dc.identifier.scopusauthoridDaniel, EE=35474017600en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats