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Article: Thapsigargin inhibits repletion of phenylephrine-sensitive intracellular Ca++ pool in vascular smooth muscles

TitleThapsigargin inhibits repletion of phenylephrine-sensitive intracellular Ca++ pool in vascular smooth muscles
Authors
Issue Date1991
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1991, v. 258 n. 3, p. 1105-1113 How to Cite?
AbstractThapsigargin (TSG), a putative selective Ca++-ATPase inhibitor, has been used to study Ca++ mobilization in many non-excitable cell types. This study aims to determine whether TSG is effective as a selective microsomal Ca++ uptake inhibitor by studying its ability to affect repletion of the phenylephrine (PE)-sensitive Ca++ pool in rat aorta and dog mesenteric artery evaluated by contractility studies. TSG caused a concentration-dependent contraction that was dependent on the concentration of extracellular Ca++. Ca++ influx promoted by TSG was found to occur mostly through L-type Ca++ channels in the dog mesenteric artery but not in the rat aorta. When arterial rings, depleted to their PE-sensitive internal store, were allowed to replete their stores in normal Krebs' solution or in the presence of elevated K+ levels, it was found that repletion was significantly enhanced in the presence of elevated K+. In TSG-treated rings, however, repletion was significantly inhibited under both conditions as indicated by the subsequent PE-induced contraction in Ca++-free medium. While the rate of contraction induced by elevated K+ levels was slow immediately after pool depletion in controls, it was rapid in TSG-treated arterial rings. The slow onset of K+ contraction may reflect Ca++ uptake in the pool which was absent in TSG-treated arteries. Differences in the behavior of the two arteries were noted and these may reflect differences in the size of their Ca++ store and their coupling to the extracellular space. Single cells isolated from the dog mesenteric artery were also found to shorten in response to TSG to an amount comparable with that obtained from whole tissue experiments. In conclusion, the findings of this study showed that TSG was effective in preventing the repletion of a PE-sensitive internal Ca++ store. These results are consistent with its proposed inhibitory action on the microsomal Ca++-transport ATPase activity.
Persistent Identifierhttp://hdl.handle.net/10722/171559
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLow, AMen_US
dc.contributor.authorGaspar, Ven_US
dc.contributor.authorKwan, CYen_US
dc.contributor.authorDarby, PJen_US
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorDaniel, EEen_US
dc.date.accessioned2012-10-30T06:15:41Z-
dc.date.available2012-10-30T06:15:41Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1991, v. 258 n. 3, p. 1105-1113en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/171559-
dc.description.abstractThapsigargin (TSG), a putative selective Ca++-ATPase inhibitor, has been used to study Ca++ mobilization in many non-excitable cell types. This study aims to determine whether TSG is effective as a selective microsomal Ca++ uptake inhibitor by studying its ability to affect repletion of the phenylephrine (PE)-sensitive Ca++ pool in rat aorta and dog mesenteric artery evaluated by contractility studies. TSG caused a concentration-dependent contraction that was dependent on the concentration of extracellular Ca++. Ca++ influx promoted by TSG was found to occur mostly through L-type Ca++ channels in the dog mesenteric artery but not in the rat aorta. When arterial rings, depleted to their PE-sensitive internal store, were allowed to replete their stores in normal Krebs' solution or in the presence of elevated K+ levels, it was found that repletion was significantly enhanced in the presence of elevated K+. In TSG-treated rings, however, repletion was significantly inhibited under both conditions as indicated by the subsequent PE-induced contraction in Ca++-free medium. While the rate of contraction induced by elevated K+ levels was slow immediately after pool depletion in controls, it was rapid in TSG-treated arterial rings. The slow onset of K+ contraction may reflect Ca++ uptake in the pool which was absent in TSG-treated arteries. Differences in the behavior of the two arteries were noted and these may reflect differences in the size of their Ca++ store and their coupling to the extracellular space. Single cells isolated from the dog mesenteric artery were also found to shorten in response to TSG to an amount comparable with that obtained from whole tissue experiments. In conclusion, the findings of this study showed that TSG was effective in preventing the repletion of a PE-sensitive internal Ca++ store. These results are consistent with its proposed inhibitory action on the microsomal Ca++-transport ATPase activity.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshIntracellular Fluid - Metabolismen_US
dc.subject.meshIsotonic Solutionsen_US
dc.subject.meshKineticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMesenteric Arteries - Drug Effects - Physiologyen_US
dc.subject.meshMuscle Contraction - Drug Effects - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshSarcoplasmic Reticulum - Drug Effects - Metabolismen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshTerpenes - Pharmacologyen_US
dc.subject.meshThapsigarginen_US
dc.titleThapsigargin inhibits repletion of phenylephrine-sensitive intracellular Ca++ pool in vascular smooth musclesen_US
dc.typeArticleen_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.pmid1890615-
dc.identifier.scopuseid_2-s2.0-0026048170en_US
dc.identifier.volume258en_US
dc.identifier.issue3en_US
dc.identifier.spage1105en_US
dc.identifier.epage1113en_US
dc.identifier.isiWOS:A1991GF68800052-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLow, AM=7102950219en_US
dc.identifier.scopusauthoridGaspar, V=7003585316en_US
dc.identifier.scopusauthoridKwan, CY=7201421224en_US
dc.identifier.scopusauthoridDarby, PJ=7003431034en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridDaniel, EE=35474017600en_US

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