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- Scopus: eid_2-s2.0-0021340657
- PMID: 6325664
- WOS: WOS:A1984SR58900014
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Article: Neurogenic cholinergic prejunctional inhibition of sympathetic beta adrenergic relaxation in the canine coronary artery
Title | Neurogenic cholinergic prejunctional inhibition of sympathetic beta adrenergic relaxation in the canine coronary artery |
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Authors | |
Issue Date | 1984 |
Publisher | American 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, 1984, v. 229 n. 2, p. 417-421 How to Cite? |
Abstract | Electrical stimulation of isolated canine coronary arteries causes release of norepinephrine and subsequent relaxation by activation of beta adrenoceptors. The purpose of the present study was to determine if this beta adrenergic relaxation was influenced by a concomitant release of acetylcholine. Rings of epicardial coronary arteries of the dog were studied in organ chambers filled with physiological salt solution. The tetrodotoxin-sensitive, beta adrenergically mediated relaxation induced by electrical stimulation was studied during contractions evoked by prostaglandin F(2α). The relaxation to low-frequency stimulation was inhibited and augmented, respectively, by acetylcholine and atropine, suggesting that release of acetylcholine may modulate the beta adrenergic response to sympathetic nerve stimulation. The relaxation caused by high-frequency stimulation was not affected by atropine or by removal of the endothelium, indicating that endogenously released acetylcholine does not act directly on the smooth muscle or initiate an endothelium-dependent vasodilator response. In superfused strips of coronary artery preincubated in [3H]norepinephrine, acetylcholine depressed the stimulated overflow of [3H]norepinephrine, indicating prejunctional cholinergic receptors on adrenergic nerve endings. Atropine augmented the overflow, suggesting that endogenous acetylcholine, released during stimulation, inhibits the release of norepinephrine. These observations suggest that prejunctional inhibition of norepinephrine release, which limits the sympathetic beta adrenergic relaxation of the smooth muscle, is the primary neurogenic cholirergic effect in canine epicardial coronary arteries. |
Persistent Identifier | http://hdl.handle.net/10722/170743 |
ISSN | 2023 Impact Factor: 3.1 2023 SCImago Journal Rankings: 0.829 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Cohen, RA | en_US |
dc.contributor.author | Shepherd, JT | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:10:40Z | - |
dc.date.available | 2012-10-30T06:10:40Z | - |
dc.date.issued | 1984 | en_US |
dc.identifier.citation | Journal Of Pharmacology And Experimental Therapeutics, 1984, v. 229 n. 2, p. 417-421 | en_US |
dc.identifier.issn | 0022-3565 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170743 | - |
dc.description.abstract | Electrical stimulation of isolated canine coronary arteries causes release of norepinephrine and subsequent relaxation by activation of beta adrenoceptors. The purpose of the present study was to determine if this beta adrenergic relaxation was influenced by a concomitant release of acetylcholine. Rings of epicardial coronary arteries of the dog were studied in organ chambers filled with physiological salt solution. The tetrodotoxin-sensitive, beta adrenergically mediated relaxation induced by electrical stimulation was studied during contractions evoked by prostaglandin F(2α). The relaxation to low-frequency stimulation was inhibited and augmented, respectively, by acetylcholine and atropine, suggesting that release of acetylcholine may modulate the beta adrenergic response to sympathetic nerve stimulation. The relaxation caused by high-frequency stimulation was not affected by atropine or by removal of the endothelium, indicating that endogenously released acetylcholine does not act directly on the smooth muscle or initiate an endothelium-dependent vasodilator response. In superfused strips of coronary artery preincubated in [3H]norepinephrine, acetylcholine depressed the stimulated overflow of [3H]norepinephrine, indicating prejunctional cholinergic receptors on adrenergic nerve endings. Atropine augmented the overflow, suggesting that endogenous acetylcholine, released during stimulation, inhibits the release of norepinephrine. These observations suggest that prejunctional inhibition of norepinephrine release, which limits the sympathetic beta adrenergic relaxation of the smooth muscle, is the primary neurogenic cholirergic effect in canine epicardial coronary arteries. | en_US |
dc.language | eng | en_US |
dc.publisher | American Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org | en_US |
dc.relation.ispartof | Journal of Pharmacology and Experimental Therapeutics | en_US |
dc.subject.mesh | Acetylcholine - Pharmacology - Secretion | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Atropine - Pharmacology | en_US |
dc.subject.mesh | Coronary Vessels - Innervation - Physiology | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Muscle Relaxation | en_US |
dc.subject.mesh | Neural Inhibition | en_US |
dc.subject.mesh | Parasympathetic Nervous System - Physiology | en_US |
dc.subject.mesh | Physostigmine - Pharmacology | en_US |
dc.subject.mesh | Receptors, Adrenergic, Beta - Physiology | en_US |
dc.subject.mesh | Sympathetic Nervous System - Physiology | en_US |
dc.title | Neurogenic cholinergic prejunctional inhibition of sympathetic beta adrenergic relaxation in the canine coronary artery | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 6325664 | - |
dc.identifier.scopus | eid_2-s2.0-0021340657 | en_US |
dc.identifier.volume | 229 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 417 | en_US |
dc.identifier.epage | 421 | en_US |
dc.identifier.isi | WOS:A1984SR58900014 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Cohen, RA=35562815800 | en_US |
dc.identifier.scopusauthorid | Shepherd, JT=7401742522 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0022-3565 | - |