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Article: Internal calcium stores and norepinephrine overflow from isolated, field stimulated rat vas deferens

TitleInternal calcium stores and norepinephrine overflow from isolated, field stimulated rat vas deferens
Authors
Issue Date1996
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1996, v. 58 n. 8, p. PL123-PL129 How to Cite?
AbstractRyanodine has been shown to selectively inhibit the initial phase of contraction of rat vas deferens smooth muscle stimulated by endogenous release of norepinephrine (NE) (1), and part of this effect could be pre-junctional. To assess this, its effect on NE overflow was measured in the same preparation. NE overflow from electrical field-stimulated isolated rat vas deferens was quantified by electrochemical detection using HPLC. In order to limit pre-junctional autoregulatory mechanisms, α2-adrenergic receptors were blocked and P(2x) purinergic receptors were desensitized. In these experimental conditions, NE overflow was directly proportional to extracellular Ca2+ concentration. Ryanodine only induced a modest decrease in NE overflow. Cyclopiazonic acid (CPA), an inhibitor of sarcoplasmic reticulum Ca2+-ATPase, slightly increased NE overflow but decreased smooth muscle contraction induced by electrical field stimulation. It is concluded that part of the effect of ryanodine on field stimulation-induced contraction may be due to an inhibition of NE release, although the major inhibitory effect of this alkaloid is post junctional. For CPA, its inhibitory effect on field stimulation-induced contraction is entirely postjunctional. Its effect on NE overflow suggests that, in this preparation, internal Ca2+ stores could function to accelerate termination of neurotransmitter release by sequestering cytosolic Ca2+.
Persistent Identifierhttp://hdl.handle.net/10722/171720
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
References

 

DC FieldValueLanguage
dc.contributor.authorBourreau, JPen_US
dc.date.accessioned2012-10-30T06:16:36Z-
dc.date.available2012-10-30T06:16:36Z-
dc.date.issued1996en_US
dc.identifier.citationLife Sciences, 1996, v. 58 n. 8, p. PL123-PL129en_US
dc.identifier.issn0024-3205en_US
dc.identifier.urihttp://hdl.handle.net/10722/171720-
dc.description.abstractRyanodine has been shown to selectively inhibit the initial phase of contraction of rat vas deferens smooth muscle stimulated by endogenous release of norepinephrine (NE) (1), and part of this effect could be pre-junctional. To assess this, its effect on NE overflow was measured in the same preparation. NE overflow from electrical field-stimulated isolated rat vas deferens was quantified by electrochemical detection using HPLC. In order to limit pre-junctional autoregulatory mechanisms, α2-adrenergic receptors were blocked and P(2x) purinergic receptors were desensitized. In these experimental conditions, NE overflow was directly proportional to extracellular Ca2+ concentration. Ryanodine only induced a modest decrease in NE overflow. Cyclopiazonic acid (CPA), an inhibitor of sarcoplasmic reticulum Ca2+-ATPase, slightly increased NE overflow but decreased smooth muscle contraction induced by electrical field stimulation. It is concluded that part of the effect of ryanodine on field stimulation-induced contraction may be due to an inhibition of NE release, although the major inhibitory effect of this alkaloid is post junctional. For CPA, its inhibitory effect on field stimulation-induced contraction is entirely postjunctional. Its effect on NE overflow suggests that, in this preparation, internal Ca2+ stores could function to accelerate termination of neurotransmitter release by sequestering cytosolic Ca2+.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_US
dc.relation.ispartofLife Sciencesen_US
dc.rightsLife Sciences. Copyright © Elsevier Inc.-
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolism - Pharmacologyen_US
dc.subject.meshCalcium-Transporting Atpases - Antagonists & Inhibitorsen_US
dc.subject.meshChromatography, High Pressure Liquiden_US
dc.subject.meshCytosol - Metabolismen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Drug Effects - Physiologyen_US
dc.subject.meshNorepinephrine - Analysis - Secretionen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshRyanodine - Pharmacologyen_US
dc.subject.meshSarcoplasmic Reticulum - Enzymologyen_US
dc.subject.meshVas Deferens - Drug Effects - Physiology - Secretionen_US
dc.titleInternal calcium stores and norepinephrine overflow from isolated, field stimulated rat vas deferensen_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.doi10.1016/S0024-3205(96)80012-9en_US
dc.identifier.pmid8594311-
dc.identifier.scopuseid_2-s2.0-0342995795en_US
dc.identifier.hkuros25740-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0342995795&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume58en_US
dc.identifier.issue8en_US
dc.identifier.spagePL123en_US
dc.identifier.epagePL129en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US

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