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Article: Effects of moderate acidosis on adrenergic neurotransmission in canine saphenous veins

TitleEffects of moderate acidosis on adrenergic neurotransmission in canine saphenous veins
Authors
Issue Date1978
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, 1978, v. 206 n. 1, p. 105-114 How to Cite?
AbstractLocal acidosis depresses vascular smooth muscle reactivity. Experiments were performed to determine whether moderate acidosis also affects the release of norepinephrine in the blood vessel wall. Helical strips of dog saphenous veins were mounted for isometric tension recording; moderate metabolic acidosis (from pH 7.4 to 7.1) was obtained by lowering the HCO3 - concentration of the Krebs-Ringer solution at constant PCO2. Acidosis significantly reduced the contractile responses to sympathetic nerve stimulation (1-10 Hz), but not those to exogenous norepinephrine (10-8 - 10-4 M). The blocker of neuronal reuptake, cocaine (3 x 10-5 M), did not affect the depressant effect of acidosis on the response to nerve stimulation. Strips were incubated in solutions containing [3H]norepinephrine and mounted for superfusion and isometric tension recording; the overflow of [3H]norepinephrine and its metabolites in the superfusate was determined by column chromatography. In control strips, acidosis caused relaxation during nerve stimulation, but did not significantly alter the evoked release of labeled transmitter; by contrast, in strips treated with cocaine, acidosis depressed the contractile response and the overflow of [3H]norepinephrine to the same extent. In the absence of cocaine, acidosis depressed the release of norepinephrine evoked by 50 mEq/l of K+, but not its displacement by 6 x 10-5 M tyramine. Acidosis significantly depressed the tissue uptake of [3H]norepinephrine, determined by extraction and column chromatography; it did not significantly alter the inhibitory effect of cocaine on [3H]norepinephrine uptake. These experiments provide direct evidence that moderate variations in extracellular pH can inhibit the evoked release of norepinephrine and suggest that local acidosis may participate in the functional disconnection of the blood vessels of metabolically active tissues from sympathetic control. They further support the concept that there is a temporal dissociation between the release of norepinephrine and its reuptake by the adrenergic nerve endings.
Persistent Identifierhttp://hdl.handle.net/10722/170559
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVerbeuren, TJen_US
dc.contributor.authorJanssens, WJen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:09:57Z-
dc.date.available2012-10-30T06:09:57Z-
dc.date.issued1978en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1978, v. 206 n. 1, p. 105-114en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170559-
dc.description.abstractLocal acidosis depresses vascular smooth muscle reactivity. Experiments were performed to determine whether moderate acidosis also affects the release of norepinephrine in the blood vessel wall. Helical strips of dog saphenous veins were mounted for isometric tension recording; moderate metabolic acidosis (from pH 7.4 to 7.1) was obtained by lowering the HCO3 - concentration of the Krebs-Ringer solution at constant PCO2. Acidosis significantly reduced the contractile responses to sympathetic nerve stimulation (1-10 Hz), but not those to exogenous norepinephrine (10-8 - 10-4 M). The blocker of neuronal reuptake, cocaine (3 x 10-5 M), did not affect the depressant effect of acidosis on the response to nerve stimulation. Strips were incubated in solutions containing [3H]norepinephrine and mounted for superfusion and isometric tension recording; the overflow of [3H]norepinephrine and its metabolites in the superfusate was determined by column chromatography. In control strips, acidosis caused relaxation during nerve stimulation, but did not significantly alter the evoked release of labeled transmitter; by contrast, in strips treated with cocaine, acidosis depressed the contractile response and the overflow of [3H]norepinephrine to the same extent. In the absence of cocaine, acidosis depressed the release of norepinephrine evoked by 50 mEq/l of K+, but not its displacement by 6 x 10-5 M tyramine. Acidosis significantly depressed the tissue uptake of [3H]norepinephrine, determined by extraction and column chromatography; it did not significantly alter the inhibitory effect of cocaine on [3H]norepinephrine uptake. These experiments provide direct evidence that moderate variations in extracellular pH can inhibit the evoked release of norepinephrine and suggest that local acidosis may participate in the functional disconnection of the blood vessels of metabolically active tissues from sympathetic control. They further support the concept that there is a temporal dissociation between the release of norepinephrine and its reuptake by the adrenergic nerve endings.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.meshAcidosis - Metabolism - Physiopathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Vessels - Innervation - Metabolism - Physiopathologyen_US
dc.subject.meshDogsen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscle, Smooth - Physiopathologyen_US
dc.subject.meshNorepinephrine - Metabolismen_US
dc.subject.meshSaphenous Vein - Innervation - Metabolism - Physiopathologyen_US
dc.subject.meshSympathetic Nervous System - Physiopathologyen_US
dc.subject.meshSynaptic Transmissionen_US
dc.titleEffects of moderate acidosis on adrenergic neurotransmission in canine saphenous veinsen_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.pmid207858-
dc.identifier.scopuseid_2-s2.0-0018193971en_US
dc.identifier.volume206en_US
dc.identifier.issue1en_US
dc.identifier.spage105en_US
dc.identifier.epage114en_US
dc.identifier.isiWOS:A1978FK52700013-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVerbeuren, TJ=7007006534en_US
dc.identifier.scopusauthoridJanssens, WJ=7006876881en_US
dc.identifier.scopusauthoridVanHoutte, PM=7202304247en_US

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