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Article: Inhibition of adrenergic neurotransmission in isolated veins of the dog by potassium ions

TitleInhibition of adrenergic neurotransmission in isolated veins of the dog by potassium ions
Authors
Issue Date1975
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1975, v. 246 n. 2, p. 479-500 How to Cite?
AbstractIn the intact organism, an increase in K+ concentration decreases the reactivity of blood vessels to sympathetic stimulation. The present experiments were designed to determine whether or not K+ interferes with adrenergic neurotransmission. Helical strips cut from dogs' saphenous veins were incubated in Krebs Ringer solution containing [7 3H]norepinephrine (5 x 10-8 g/ml). The preparations were mounted for superfusion and isometric tension recording; the superfusate was collected for estimation of total radioactivity and for chromatographic separation of 3H labelled norepinephrine and metabolites. Supramaximal electric stimulation (5 Hz, 9 V, 2 msec) increased the tension and the [3H]norepinephrine efflux. Increasing the K+ concentration from 5.9 to 10, 15, and 20 m equiv/l. caused a progressive depression of these contractions and diminished the total 3H efflux in proportion to the relaxation; the decrease in 3H efflux reflected a decrease in intact [3H]norepinephrine. The same increase in K+ concentration did not alter basal tension or basal 3H efflux. Addition of tyramine (4 x 10-6 g/ml. min) to the superfusate augmented both the tension and the efflux, but these actions were not depressed by increasing the K+ concentration. Cocaine, phentolamine, and phenoxybenzamine did not prevent the depression by K+ of the response to electric stimulation. These experiments show that K+ causes relaxation of venous smooth muscle constricted by sympathetic stimulation and does so by inhibiting the release of norepinephrine from nerve endings. By contrast, K+ does not inhibit norepinephrine release in response to tyramine. During submaximal electric stimulation (5 Hz, 1.8-3 V, 2 msec), increasing the K+ concentration from 5.9 to 10 and 15 m equiv/l. potentiated the contractions and increased the [3H]norepinephrine efflux; at 20 m equiv/l., K+ caused transient increases in tension and 3H efflux followed by relaxation and decreased norepinephrine release. After addition of cocaine (10-5 g/ml. min), K+ only caused relaxation and decrease in 3H efflux, showing that, in addition to inhibition of norepinephrine release, K+ also inhibits the reuptake process. In higher concentrations (40 m equiv/l.), K+ caused both a liberation of norepinephrine and a direct activation of the smooth muscle cells.
Persistent Identifierhttp://hdl.handle.net/10722/170507
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLorenz, RRen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:09:44Z-
dc.date.available2012-10-30T06:09:44Z-
dc.date.issued1975en_US
dc.identifier.citationJournal Of Physiology, 1975, v. 246 n. 2, p. 479-500en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/170507-
dc.description.abstractIn the intact organism, an increase in K+ concentration decreases the reactivity of blood vessels to sympathetic stimulation. The present experiments were designed to determine whether or not K+ interferes with adrenergic neurotransmission. Helical strips cut from dogs' saphenous veins were incubated in Krebs Ringer solution containing [7 3H]norepinephrine (5 x 10-8 g/ml). The preparations were mounted for superfusion and isometric tension recording; the superfusate was collected for estimation of total radioactivity and for chromatographic separation of 3H labelled norepinephrine and metabolites. Supramaximal electric stimulation (5 Hz, 9 V, 2 msec) increased the tension and the [3H]norepinephrine efflux. Increasing the K+ concentration from 5.9 to 10, 15, and 20 m equiv/l. caused a progressive depression of these contractions and diminished the total 3H efflux in proportion to the relaxation; the decrease in 3H efflux reflected a decrease in intact [3H]norepinephrine. The same increase in K+ concentration did not alter basal tension or basal 3H efflux. Addition of tyramine (4 x 10-6 g/ml. min) to the superfusate augmented both the tension and the efflux, but these actions were not depressed by increasing the K+ concentration. Cocaine, phentolamine, and phenoxybenzamine did not prevent the depression by K+ of the response to electric stimulation. These experiments show that K+ causes relaxation of venous smooth muscle constricted by sympathetic stimulation and does so by inhibiting the release of norepinephrine from nerve endings. By contrast, K+ does not inhibit norepinephrine release in response to tyramine. During submaximal electric stimulation (5 Hz, 1.8-3 V, 2 msec), increasing the K+ concentration from 5.9 to 10 and 15 m equiv/l. potentiated the contractions and increased the [3H]norepinephrine efflux; at 20 m equiv/l., K+ caused transient increases in tension and 3H efflux followed by relaxation and decreased norepinephrine release. After addition of cocaine (10-5 g/ml. min), K+ only caused relaxation and decrease in 3H efflux, showing that, in addition to inhibition of norepinephrine release, K+ also inhibits the reuptake process. In higher concentrations (40 m equiv/l.), K+ caused both a liberation of norepinephrine and a direct activation of the smooth muscle cells.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Transport, Active - Drug Effectsen_US
dc.subject.meshCocaine - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshMuscle, Smooth - Drug Effectsen_US
dc.subject.meshNorepinephrine - Metabolismen_US
dc.subject.meshPhenoxybenzamine - Pharmacologyen_US
dc.subject.meshPhentolamine - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshSaphenous Vein - Drug Effects - Innervation - Metabolismen_US
dc.subject.meshSympathetic Nervous System - Physiologyen_US
dc.subject.meshSynaptic Transmission - Drug Effectsen_US
dc.subject.meshTyramine - Pharmacologyen_US
dc.titleInhibition of adrenergic neurotransmission in isolated veins of the dog by potassium ionsen_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.pmid167162-
dc.identifier.scopuseid_2-s2.0-0016715040en_US
dc.identifier.volume246en_US
dc.identifier.issue2en_US
dc.identifier.spage479en_US
dc.identifier.epage500en_US
dc.identifier.isiWOS:A1975W282600011-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLorenz, RR=7402095192en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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