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Article: Local modulation of adrenergic neurotransmission

TitleLocal modulation of adrenergic neurotransmission
Authors
Issue Date1981
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.org
Citation
Circulation, 1981, v. 64 n. 4, p. 655-666 How to Cite?
AbstractThe cardiovascular reflexes, by regulating the traffic in the sympathetic nerves, govern the amount of norepinephrine released from the nerve endings. However, the final adjustment in the amount of neurotransmitter available to activate the β1 receptors in the heart and the α receptors in the blood vessels takes place at the sympathetic neuroeffector junction. Thus, a decrease in pH, hyperosmolarity, moderate increases in the concentration of K+ ion, adenosine and adenine nucleotides depress the release of norepinephrine at any given level of sympathetic nerve activity. These metabolic changes, which occur in active tissues, and in particular in adenosine, have been proposed as mediators of the accompanying local hyperemia. In addition, they apparently facilitate this local dilation by disconnecting the blood vessels in the active tissues from sympathetic control. Acetylcholine, histamine and 5-hydroxytryptamine are present in and around certain blood vessels and can activate specific receptors on the prejunctional fibers and cause vasodilation by reducing the output of neurotransmitter. Some of the norepinephrine released into the synaptic cleft may depress its continued release by activating prejunctional α receptors. In contrast, angiotensin II, by a local action on the nerve endings, can augment the release of transmitter. Decreases in local temperature reduce transmitter release but augment the affinity of the postjunctional α receptors for norepinephrine. The role of these local events at the neuroeffector junction, their physiologic significance and potential clinical importance are discussed in this review.
Persistent Identifierhttp://hdl.handle.net/10722/170635
ISSN
2015 Impact Factor: 17.047
2015 SCImago Journal Rankings: 7.853
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShepherd, JTen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:14Z-
dc.date.available2012-10-30T06:10:14Z-
dc.date.issued1981en_US
dc.identifier.citationCirculation, 1981, v. 64 n. 4, p. 655-666en_US
dc.identifier.issn0009-7322en_US
dc.identifier.urihttp://hdl.handle.net/10722/170635-
dc.description.abstractThe cardiovascular reflexes, by regulating the traffic in the sympathetic nerves, govern the amount of norepinephrine released from the nerve endings. However, the final adjustment in the amount of neurotransmitter available to activate the β1 receptors in the heart and the α receptors in the blood vessels takes place at the sympathetic neuroeffector junction. Thus, a decrease in pH, hyperosmolarity, moderate increases in the concentration of K+ ion, adenosine and adenine nucleotides depress the release of norepinephrine at any given level of sympathetic nerve activity. These metabolic changes, which occur in active tissues, and in particular in adenosine, have been proposed as mediators of the accompanying local hyperemia. In addition, they apparently facilitate this local dilation by disconnecting the blood vessels in the active tissues from sympathetic control. Acetylcholine, histamine and 5-hydroxytryptamine are present in and around certain blood vessels and can activate specific receptors on the prejunctional fibers and cause vasodilation by reducing the output of neurotransmitter. Some of the norepinephrine released into the synaptic cleft may depress its continued release by activating prejunctional α receptors. In contrast, angiotensin II, by a local action on the nerve endings, can augment the release of transmitter. Decreases in local temperature reduce transmitter release but augment the affinity of the postjunctional α receptors for norepinephrine. The role of these local events at the neuroeffector junction, their physiologic significance and potential clinical importance are discussed in this review.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.orgen_US
dc.relation.ispartofCirculationen_US
dc.subject.meshAcetylcholine - Blooden_US
dc.subject.meshAcidosis - Metabolismen_US
dc.subject.meshAdenine Nucleotides - Metabolismen_US
dc.subject.meshAdenosine - Metabolismen_US
dc.subject.meshAngiotensin Ii - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshHistamine - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshNerve Endings - Metabolismen_US
dc.subject.meshOsmolar Concentrationen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Alphaen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.subject.meshSympathomimetics - Pharmacologyen_US
dc.subject.meshSynaptic Transmissionen_US
dc.subject.meshTemperatureen_US
dc.subject.meshVasodilationen_US
dc.titleLocal modulation of adrenergic neurotransmissionen_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.doi10.1161/01.CIR.64.4.655-
dc.identifier.pmid6268334-
dc.identifier.scopuseid_2-s2.0-0019442014en_US
dc.identifier.volume64en_US
dc.identifier.issue4en_US
dc.identifier.spage655en_US
dc.identifier.epage666en_US
dc.identifier.isiWOS:A1981MH62300001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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