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Article: Interaction between Na+,K+ exchanges and the direct inhibitory effect of acetylcholine on canine femoral arteries

TitleInteraction between Na+,K+ exchanges and the direct inhibitory effect of acetylcholine on canine femoral arteries
Authors
Issue Date1980
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1980, v. 46 n. 6, p. 826-836 How to Cite?
AbstractWe studied the mechanism by which acetylcholine causes relaxation of vascular smooth muscle cells. Isolated rings of femoral arteries of the dog were mounted for isometric tension recording in organ chambers filled with Krebs-Ringer's solution. This preparation was used because it is not densely innervated, and it is sensitive to the direct inhibitory effect of acetylcholine. Acetylcholine caused dose-dependent relaxation during contractions evoked by norepinephrine and potassium (24 mEq/liter); at higher potassium concentrations, the inhibitory effect of acetylcholine was progressively depressed. The inhibitory effect of acetylcholine was not altered by phentolamine, propranolol, or hexamethonium; it was inhibited by atropine, indicating its muscarinic nature. Anoxia, moderate cooling, ouabain, reduction of the potassium concentration, or reduction of the sodium concentration abolished the acetylcholine-induced relaxation. Preparations incubated in low potassium solution and made to contract with norepinephrine responded to an increase in potassium concentration with transient relaxations. These were depressed by anoxia and abolished by moderate cooling, ouabain, and reduction of the sodium concentration. Verapamil reduced the potassium-induced relaxation, but not that caused by acetylcholine. These results suggest that Na+,K+-ATPase -ATPase is involved indirectly in the inhibitory effect of acetylcholine on vascular smooth muscle cells.
Persistent Identifierhttp://hdl.handle.net/10722/170617
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDe Mey, JGen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:09Z-
dc.date.available2012-10-30T06:10:09Z-
dc.date.issued1980en_US
dc.identifier.citationCirculation Research, 1980, v. 46 n. 6, p. 826-836en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170617-
dc.description.abstractWe studied the mechanism by which acetylcholine causes relaxation of vascular smooth muscle cells. Isolated rings of femoral arteries of the dog were mounted for isometric tension recording in organ chambers filled with Krebs-Ringer's solution. This preparation was used because it is not densely innervated, and it is sensitive to the direct inhibitory effect of acetylcholine. Acetylcholine caused dose-dependent relaxation during contractions evoked by norepinephrine and potassium (24 mEq/liter); at higher potassium concentrations, the inhibitory effect of acetylcholine was progressively depressed. The inhibitory effect of acetylcholine was not altered by phentolamine, propranolol, or hexamethonium; it was inhibited by atropine, indicating its muscarinic nature. Anoxia, moderate cooling, ouabain, reduction of the potassium concentration, or reduction of the sodium concentration abolished the acetylcholine-induced relaxation. Preparations incubated in low potassium solution and made to contract with norepinephrine responded to an increase in potassium concentration with transient relaxations. These were depressed by anoxia and abolished by moderate cooling, ouabain, and reduction of the sodium concentration. Verapamil reduced the potassium-induced relaxation, but not that caused by acetylcholine. These results suggest that Na+,K+-ATPase -ATPase is involved indirectly in the inhibitory effect of acetylcholine on vascular smooth muscle cells.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshDogsen_US
dc.subject.meshFemoral Artery - Drug Effectsen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshOuabain - Pharmacologyen_US
dc.subject.meshOxygen - Metabolismen_US
dc.subject.meshPhosphodiesterase Inhibitors - Pharmacologyen_US
dc.subject.meshPhysostigmine - Pharmacologyen_US
dc.subject.meshPotassium - Metabolismen_US
dc.subject.meshReceptors, Adrenergic - Drug Effectsen_US
dc.subject.meshReceptors, Cholinergic - Drug Effectsen_US
dc.subject.meshSodium - Metabolismen_US
dc.subject.meshTemperatureen_US
dc.titleInteraction between Na+,K+ exchanges and the direct inhibitory effect of acetylcholine on canine femoral arteriesen_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.pmid7379248-
dc.identifier.scopuseid_2-s2.0-0019199687en_US
dc.identifier.volume46en_US
dc.identifier.issue6en_US
dc.identifier.spage826en_US
dc.identifier.epage836en_US
dc.identifier.isiWOS:A1980JW90400012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDe Mey, JG=7101918486en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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