File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The effects of acetylstrophanthidin and ouabain on the sympathetic adrenergic neuroeffector junction in canine vascular smooth muscle

TitleThe effects of acetylstrophanthidin and ouabain on the sympathetic adrenergic neuroeffector junction in canine vascular smooth muscle
Authors
Issue Date1980
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1980, v. 47 n. 6, p. 845-854 How to Cite?
AbstractWe performed experiments to determine the effects of acetylstrophanthidin (ACS) and ouabain on the adrenergic neuroeffector junction in dog saphenous veins. In quiescent strips incubated with 3H-norepinephrine (3H-NE), the drugs caused contraction and a progressive increase in overflow of 3H-NE and O-methylated metabolites; 3,4-dihydroxyphenylglycol (DOPEG) decreased. Tissue uptake of 3H-NE was partially inhibited. After surgical sympathectomy, both contraction and 3H-NE overflow were markedly attenuated. Following chemical sympathectomy with 6-hydroxydopamine, ouabain contractions were 11% of control, whereas the contractions due to exogenous norepinephrine were exaggerated. The initial overflow of 3H-NE was unaffected by tetrodoxin, but the later and larger overflow with prolonged exposure was depressed. The former occurred in the absence of CA2+, but the latter was Ca2+ dependent. Inhibition of the neuronal amine carrier by cocaine or desipramine and blockade of the neuronal α-adrenoreceptors with phentolamine or phenoxybenzamine attenuated the release of 3H-NE evoked by ACS and ouabain. During electrical stimulation, ACS augmented the overflow of 3H-NE. This was attenuated by cocaine, desipramine, and the α-adrenolytic drugs. ACS, like pargyline, augmented the overflow of 3H-NE evoked by tyramine and depressed that of DOPEG. These experiments suggest that acetylstrophanthidin and ouabain cause contraction of vascular smooth muscle by displacement of norepinephrine from neuronal stores, reduce neuronal monoamine oxidase activity, facilitate and may trigger Ca2+-dependent exocytotic release of norepinephrine, partially inhibit the neuronal amine carrier mechanism but do not interfere with extraneuronal disposition of norepinephrine, and, finally may have unexplained interactions with prejunctional α-adrenoceptors.
Persistent Identifierhttp://hdl.handle.net/10722/170618
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLorenz, RRen_US
dc.contributor.authorPowis, DAen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorShepherd, JTen_US
dc.date.accessioned2012-10-30T06:10:10Z-
dc.date.available2012-10-30T06:10:10Z-
dc.date.issued1980en_US
dc.identifier.citationCirculation Research, 1980, v. 47 n. 6, p. 845-854en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170618-
dc.description.abstractWe performed experiments to determine the effects of acetylstrophanthidin (ACS) and ouabain on the adrenergic neuroeffector junction in dog saphenous veins. In quiescent strips incubated with 3H-norepinephrine (3H-NE), the drugs caused contraction and a progressive increase in overflow of 3H-NE and O-methylated metabolites; 3,4-dihydroxyphenylglycol (DOPEG) decreased. Tissue uptake of 3H-NE was partially inhibited. After surgical sympathectomy, both contraction and 3H-NE overflow were markedly attenuated. Following chemical sympathectomy with 6-hydroxydopamine, ouabain contractions were 11% of control, whereas the contractions due to exogenous norepinephrine were exaggerated. The initial overflow of 3H-NE was unaffected by tetrodoxin, but the later and larger overflow with prolonged exposure was depressed. The former occurred in the absence of CA2+, but the latter was Ca2+ dependent. Inhibition of the neuronal amine carrier by cocaine or desipramine and blockade of the neuronal α-adrenoreceptors with phentolamine or phenoxybenzamine attenuated the release of 3H-NE evoked by ACS and ouabain. During electrical stimulation, ACS augmented the overflow of 3H-NE. This was attenuated by cocaine, desipramine, and the α-adrenolytic drugs. ACS, like pargyline, augmented the overflow of 3H-NE evoked by tyramine and depressed that of DOPEG. These experiments suggest that acetylstrophanthidin and ouabain cause contraction of vascular smooth muscle by displacement of norepinephrine from neuronal stores, reduce neuronal monoamine oxidase activity, facilitate and may trigger Ca2+-dependent exocytotic release of norepinephrine, partially inhibit the neuronal amine carrier mechanism but do not interfere with extraneuronal disposition of norepinephrine, and, finally may have unexplained interactions with prejunctional α-adrenoceptors.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCocaine - Pharmacologyen_US
dc.subject.meshDesipramine - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshMuscle, Smooth, Vascularen_US
dc.subject.meshNeuroeffector Junction - Drug Effectsen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshOuabain - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic - Drug Effectsen_US
dc.subject.meshSaphenous Vein - Drug Effectsen_US
dc.subject.meshStrophanthidin - Pharmacologyen_US
dc.subject.meshSympathetic Nervous System - Drug Effectsen_US
dc.titleThe effects of acetylstrophanthidin and ouabain on the sympathetic adrenergic neuroeffector junction in canine vascular smooth muscleen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid7438335-
dc.identifier.scopuseid_2-s2.0-0019219320en_US
dc.identifier.volume47en_US
dc.identifier.issue6en_US
dc.identifier.spage845en_US
dc.identifier.epage854en_US
dc.identifier.isiWOS:A1980KU63600007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLorenz, RR=7402095192en_US
dc.identifier.scopusauthoridPowis, DA=7005973575en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats