File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Ryanodine and the adrenergic, purinergic stimulation in the rat vas deferens smooth muscle: Functional and radioligand binding studies

TitleRyanodine and the adrenergic, purinergic stimulation in the rat vas deferens smooth muscle: Functional and radioligand binding studies
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. 256 n. 3, p. 1063-1071 How to Cite?
AbstractThe distribution of [3H]ryanodine binding in subcellular fractions isolated from rat vas deferens (RVD) paralleled that of NADPH cytochrome C reductase activity indicating an endoplasmic reticulum origin of the binding sites. Scatchard analysis of [3H]ryanodine binding indicated an homogenous site with a K(d) value of 6.4 nM. The maximum number of ryanodine binding sites was 488 fmol of [3H]ryanodine per milligram of protein. Norepinephrine (NE) or ATP endogenously released after electrical field stimulation (tetrodoxin-sensitive responses), both produced a biphasic contraction of the RVD when the action of the other was blocked. When NE was the agonist (prazosin-sensitive response), the initial transient contraction was suppressed by 30 μM ryanodine whereas the secondary component was abolished by 2 μM nifedipine. When ATP was the agonist (P2 tachyphylaxis-sensitive response), both phases of the contraction were suppressed by 2 μM nifedipine. However, the initial phasic component of the contraction induced by endogenously released ATP was also inhibited by 30 μM ryanodine except at high stimulation frequency (10 Hz). Exogenously added NE and α,β methylene ATP produced concentration-dependent contractions of the RVD. The effect of both agonists was inhibited by 2 μM nifedipine whereas 30 μM ryanodine had little effect except at high concentrations of NE. We conclude that ryanodine binding sites reside in RVD endoplasmic reticulum. There was a lack of uniformity in the effect of ryanodine and nifedipine against alpha adrenoceptor stimulation and purinoceptor stimulation indicating a difference in the stimulation-contraction coupling process between these two modes of stimulation.
Persistent Identifierhttp://hdl.handle.net/10722/171553
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorZhang, ZDen_US
dc.contributor.authorLow, AMen_US
dc.contributor.authorKwan, CYen_US
dc.contributor.authorDaniel, EEen_US
dc.date.accessioned2012-10-30T06:15:39Z-
dc.date.available2012-10-30T06:15:39Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1991, v. 256 n. 3, p. 1063-1071en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/171553-
dc.description.abstractThe distribution of [3H]ryanodine binding in subcellular fractions isolated from rat vas deferens (RVD) paralleled that of NADPH cytochrome C reductase activity indicating an endoplasmic reticulum origin of the binding sites. Scatchard analysis of [3H]ryanodine binding indicated an homogenous site with a K(d) value of 6.4 nM. The maximum number of ryanodine binding sites was 488 fmol of [3H]ryanodine per milligram of protein. Norepinephrine (NE) or ATP endogenously released after electrical field stimulation (tetrodoxin-sensitive responses), both produced a biphasic contraction of the RVD when the action of the other was blocked. When NE was the agonist (prazosin-sensitive response), the initial transient contraction was suppressed by 30 μM ryanodine whereas the secondary component was abolished by 2 μM nifedipine. When ATP was the agonist (P2 tachyphylaxis-sensitive response), both phases of the contraction were suppressed by 2 μM nifedipine. However, the initial phasic component of the contraction induced by endogenously released ATP was also inhibited by 30 μM ryanodine except at high stimulation frequency (10 Hz). Exogenously added NE and α,β methylene ATP produced concentration-dependent contractions of the RVD. The effect of both agonists was inhibited by 2 μM nifedipine whereas 30 μM ryanodine had little effect except at high concentrations of NE. We conclude that ryanodine binding sites reside in RVD endoplasmic reticulum. There was a lack of uniformity in the effect of ryanodine and nifedipine against alpha adrenoceptor stimulation and purinoceptor stimulation indicating a difference in the stimulation-contraction coupling process between these two modes of stimulation.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.meshBinding Sitesen_US
dc.subject.meshCalcium - Antagonists & Inhibitorsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshKineticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Drug Effects - Metabolismen_US
dc.subject.meshNifedipine - Pharmacologyen_US
dc.subject.meshRadioligand Assayen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshReceptors, Purinergic - Drug Effectsen_US
dc.subject.meshRyanodine - Metabolism - Pharmacologyen_US
dc.subject.meshVas Deferensen_US
dc.titleRyanodine and the adrenergic, purinergic stimulation in the rat vas deferens smooth muscle: Functional and radioligand binding studiesen_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.pmid2005572-
dc.identifier.scopuseid_2-s2.0-0025868920en_US
dc.identifier.volume256en_US
dc.identifier.issue3en_US
dc.identifier.spage1063en_US
dc.identifier.epage1071en_US
dc.identifier.isiWOS:A1991FC92300035-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridZhang, ZD=8910035400en_US
dc.identifier.scopusauthoridLow, AM=7102950219en_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