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Article: Cholinergic inhibition of adrenergic transmission

TitleCholinergic inhibition of adrenergic transmission
Authors
Issue Date1977
Citation
Federation Proceedings, 1977, v. 36 n. 10, p. 2444-2449 How to Cite?
AbstractAcetylcholine has a dual direct effect on vascular smooth muscle. Low concentrations cause relaxation and high concentrations contraction of arteries; veins only contract when exposed to acetylcholine. Both the inhibitory and excitatory component are inhibited by atropine, suggesting the presence of two muscarinic receptors in vascular smooth muscle; depending on their relative distribution, relaxation, biphasic responses, or contractions are obtained. Since only arteries and arterioles are innervated by cholinergic nerves, and since only high concentrations of acetylcholine constrict arteries it is likely that in the intact organism only the relaxatory effect of acetylcholine is of importance. During sympathetic nerve stimulation, acetylcholine in concentrations causing relaxation of arterial smooth muscle reversibly inhibits adrenergic neurotransmission, by decreasing the amount of norepinephrine released by the nerve impulses. This effect can be demonstrated throughout the vascular tree, and in the intact animal. It is due to activation of muscarinic receptors resulting in hyperpolarization of the adrenergic nerve terminals. The inhibition of adrenergic neurotransmission concurs with the direct relaxatory effect of acetylcholine on arterial smooth muscle, and explains part of the potent dilator effects of the drug in the intact organism. Particularly in the case of neurogenic cholinergic vasodilatation, this mechanism must allow a very effective control, since on release of the inhibitory agonist the liberation of the excitatory transmitter is automatically interrupted.
Persistent Identifierhttp://hdl.handle.net/10722/170537
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:09:51Z-
dc.date.available2012-10-30T06:09:51Z-
dc.date.issued1977en_US
dc.identifier.citationFederation Proceedings, 1977, v. 36 n. 10, p. 2444-2449en_US
dc.identifier.issn0014-9446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170537-
dc.description.abstractAcetylcholine has a dual direct effect on vascular smooth muscle. Low concentrations cause relaxation and high concentrations contraction of arteries; veins only contract when exposed to acetylcholine. Both the inhibitory and excitatory component are inhibited by atropine, suggesting the presence of two muscarinic receptors in vascular smooth muscle; depending on their relative distribution, relaxation, biphasic responses, or contractions are obtained. Since only arteries and arterioles are innervated by cholinergic nerves, and since only high concentrations of acetylcholine constrict arteries it is likely that in the intact organism only the relaxatory effect of acetylcholine is of importance. During sympathetic nerve stimulation, acetylcholine in concentrations causing relaxation of arterial smooth muscle reversibly inhibits adrenergic neurotransmission, by decreasing the amount of norepinephrine released by the nerve impulses. This effect can be demonstrated throughout the vascular tree, and in the intact animal. It is due to activation of muscarinic receptors resulting in hyperpolarization of the adrenergic nerve terminals. The inhibition of adrenergic neurotransmission concurs with the direct relaxatory effect of acetylcholine on arterial smooth muscle, and explains part of the potent dilator effects of the drug in the intact organism. Particularly in the case of neurogenic cholinergic vasodilatation, this mechanism must allow a very effective control, since on release of the inhibitory agonist the liberation of the excitatory transmitter is automatically interrupted.en_US
dc.languageengen_US
dc.relation.ispartofFederation Proceedingsen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdrenergic Fibers - Drug Effectsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Vessels - Innervationen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Innervationen_US
dc.subject.meshNerve Endings - Drug Effectsen_US
dc.subject.meshNeural Inhibitionen_US
dc.subject.meshNorepinephrine - Metabolismen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Drug Effectsen_US
dc.subject.meshReceptors, Muscarinic - Physiologyen_US
dc.subject.meshSynaptic Transmission - Drug Effectsen_US
dc.subject.meshTyramine - Pharmacologyen_US
dc.titleCholinergic inhibition of adrenergic transmissionen_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.pmid196943-
dc.identifier.scopuseid_2-s2.0-0017700209en_US
dc.identifier.volume36en_US
dc.identifier.issue10en_US
dc.identifier.spage2444en_US
dc.identifier.epage2449en_US
dc.identifier.isiWOS:A1977DU75000025-
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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