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Article: Adrenergic neuroeffector interaction in the blood vessel wall

TitleAdrenergic neuroeffector interaction in the blood vessel wall
Authors
Issue Date1978
Citation
Federation Proceedings, 1978, v. 37 n. 2, p. 181-186 How to Cite?
AbstractMost blood vessels are supplied with adrenergic nerve fibers, which in their varicosities contain vesicles formed in the neuron cell body. The vesicles are the storage sites for norephinephrine, whether synthesized locally from tyrosine or actively taken up from the extracellular fluid by the varicosities (neuronal uptake). Norepinephrine can leave the storage sites 1) by leakage into the neuroplasm, in which case most of it is metabolized intraneuronally by monoamine oxidase; 2) by displacement with indirect sympathomimetic amines; and 3) by active release, together with dopamine-β-hydroxylase, the enzyme catalyzing the final step of the norepinephrine synthesis: this exocytotic process is triggered by an increase in neuroplasmic Ca2+ concentration resulting from neuronal membrane depolarization. The norepinephrine released into the junctional cleft from the adrenergic varicosity diffuses to the smooth muscle cells where it binds to receptor or acceptor sites on the membrane. The binding to the receptors initiates a change in the activity of the vascular smooth muscle; in most vessels the norepinephrine-receptor interaction is alpha-adrenergic and evokes a constriction. Released norepinephrine is removed by 1) neuronal uptake, 2) overflow to the extracellular fluid and the bloodstream, 3) binding to nonvascular smooth muscle structures, and 4) uptake by smooth muscle cells and subsequent metabolization by catechol-O-methyl transferase and monoamine oxidase; the relative importance of these different deactivation pathways depends mainly on anatomical factors such as density and pattern of innervation.
Persistent Identifierhttp://hdl.handle.net/10722/170552
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:09:54Z-
dc.date.available2012-10-30T06:09:54Z-
dc.date.issued1978en_US
dc.identifier.citationFederation Proceedings, 1978, v. 37 n. 2, p. 181-186en_US
dc.identifier.issn0014-9446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170552-
dc.description.abstractMost blood vessels are supplied with adrenergic nerve fibers, which in their varicosities contain vesicles formed in the neuron cell body. The vesicles are the storage sites for norephinephrine, whether synthesized locally from tyrosine or actively taken up from the extracellular fluid by the varicosities (neuronal uptake). Norepinephrine can leave the storage sites 1) by leakage into the neuroplasm, in which case most of it is metabolized intraneuronally by monoamine oxidase; 2) by displacement with indirect sympathomimetic amines; and 3) by active release, together with dopamine-β-hydroxylase, the enzyme catalyzing the final step of the norepinephrine synthesis: this exocytotic process is triggered by an increase in neuroplasmic Ca2+ concentration resulting from neuronal membrane depolarization. The norepinephrine released into the junctional cleft from the adrenergic varicosity diffuses to the smooth muscle cells where it binds to receptor or acceptor sites on the membrane. The binding to the receptors initiates a change in the activity of the vascular smooth muscle; in most vessels the norepinephrine-receptor interaction is alpha-adrenergic and evokes a constriction. Released norepinephrine is removed by 1) neuronal uptake, 2) overflow to the extracellular fluid and the bloodstream, 3) binding to nonvascular smooth muscle structures, and 4) uptake by smooth muscle cells and subsequent metabolization by catechol-O-methyl transferase and monoamine oxidase; the relative importance of these different deactivation pathways depends mainly on anatomical factors such as density and pattern of innervation.en_US
dc.languageengen_US
dc.relation.ispartofFederation Proceedingsen_US
dc.subject.meshAdrenergic Fibers - Physiologyen_US
dc.subject.meshBlood Vessels - Innervationen_US
dc.subject.meshMuscle, Smooth - Innervationen_US
dc.subject.meshNeuroeffector Junction - Physiologyen_US
dc.subject.meshNeurons - Physiologyen_US
dc.subject.meshNorepinephrine - Biosynthesis - Metabolism - Secretionen_US
dc.subject.meshSympathomimetics - Pharmacologyen_US
dc.titleAdrenergic neuroeffector interaction in the blood vessel wallen_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.pmid342279-
dc.identifier.scopuseid_2-s2.0-0017872507en_US
dc.identifier.volume37en_US
dc.identifier.issue2en_US
dc.identifier.spage181en_US
dc.identifier.epage186en_US
dc.identifier.isiWOS:A1978ER63000018-
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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