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Article: Potassium-induced release of endothelium-derived relaxing factor from canine femoral arteries

TitlePotassium-induced release of endothelium-derived relaxing factor from canine femoral arteries
Authors
Issue Date1988
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1988, v. 62 n. 6, p. 1098-1103 How to Cite?
AbstractExperiments were designed in a bioassay system to analyze the effect of elevated (from 5.9 mM to 7.5-45.9 mM) extracellular K+ concentration on the release of endothelium-derived relaxing factor. Segments of canine femoral artery with endothelium (donor segment) were mounted in an organ bath and perfused with modified Krebs-Ringer bicarbonate solution; the effluent from the donor segment was used to superfuse a canine coronary artery ring without endothelium (bioassay tissue). Elevation of perfusate K+ concentration by 1.6-15 mM by intraluminal infusion of potassium chloride upstream of the donor segment evoked further contractions of bioassay rings contracted with prostaglandin F(2α). In contrast, the bioassay rings progressively relaxed when increasing concentrations of potassium chloride (10-40 mM) were added extraluminally to the organ bath where the perfused segment was mounted. Extraluminal application of phenylephrine or prostaglandin F(2α) did not evoke relaxations in the bioassay ring. Removal of the endothelium from the donor segment or selective exposure of the segment (but not the bioassay ring) to Ca2+-deficient solution prevented the K+-induced relaxations. Treatment of the donor segment and the bioassay ring with inhibitors of known endogenous vasoactive substances (acetylcholine, norepinephrine, adenine nucleotides, and prostanoids) had no significant effect on the relaxation of the bioassay ring evoked by extraluminal application of potassium chloride. Simultaneous measurements of changes in isometric force in the donor segment and bioassay ring revealed that extraluminal elevation of K+ concentation relaxed the segments as well and that the relaxations could not be prevented by simultaneous intraluminal infusion of potassium chloride. Prolongation of the transit time between the donor segment and bioassay ring from 1 to 6 seconds depressed the relaxations of the bioassay tissue evoked by extraluminal elevation of K+ concentrations that could be prevented by superoxide dismutase (infused downstream of the donor segment). These findings indicate that K+ can stimulate the release of endothelium-derived relaxing factor from perfused canine femoral arteries but only when applied extraluminally. It is postulated that K+ triggers the release of a still unidentified mediator in the blood vessel wall that stimulates the release of the relaxing factor from the endothelial cells.
Persistent Identifierhttp://hdl.handle.net/10722/170900
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, GMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:21Z-
dc.date.available2012-10-30T06:11:21Z-
dc.date.issued1988en_US
dc.identifier.citationCirculation Research, 1988, v. 62 n. 6, p. 1098-1103en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170900-
dc.description.abstractExperiments were designed in a bioassay system to analyze the effect of elevated (from 5.9 mM to 7.5-45.9 mM) extracellular K+ concentration on the release of endothelium-derived relaxing factor. Segments of canine femoral artery with endothelium (donor segment) were mounted in an organ bath and perfused with modified Krebs-Ringer bicarbonate solution; the effluent from the donor segment was used to superfuse a canine coronary artery ring without endothelium (bioassay tissue). Elevation of perfusate K+ concentration by 1.6-15 mM by intraluminal infusion of potassium chloride upstream of the donor segment evoked further contractions of bioassay rings contracted with prostaglandin F(2α). In contrast, the bioassay rings progressively relaxed when increasing concentrations of potassium chloride (10-40 mM) were added extraluminally to the organ bath where the perfused segment was mounted. Extraluminal application of phenylephrine or prostaglandin F(2α) did not evoke relaxations in the bioassay ring. Removal of the endothelium from the donor segment or selective exposure of the segment (but not the bioassay ring) to Ca2+-deficient solution prevented the K+-induced relaxations. Treatment of the donor segment and the bioassay ring with inhibitors of known endogenous vasoactive substances (acetylcholine, norepinephrine, adenine nucleotides, and prostanoids) had no significant effect on the relaxation of the bioassay ring evoked by extraluminal application of potassium chloride. Simultaneous measurements of changes in isometric force in the donor segment and bioassay ring revealed that extraluminal elevation of K+ concentation relaxed the segments as well and that the relaxations could not be prevented by simultaneous intraluminal infusion of potassium chloride. Prolongation of the transit time between the donor segment and bioassay ring from 1 to 6 seconds depressed the relaxations of the bioassay tissue evoked by extraluminal elevation of K+ concentrations that could be prevented by superoxide dismutase (infused downstream of the donor segment). These findings indicate that K+ can stimulate the release of endothelium-derived relaxing factor from perfused canine femoral arteries but only when applied extraluminally. It is postulated that K+ triggers the release of a still unidentified mediator in the blood vessel wall that stimulates the release of the relaxing factor from the endothelial 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.meshAnimalsen_US
dc.subject.meshBiological Agents - Metabolismen_US
dc.subject.meshCalcium - Pharmacologyen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshExtracellular Spaceen_US
dc.subject.meshFemoral Artery - Metabolismen_US
dc.subject.meshNitric Oxideen_US
dc.subject.meshOsmolar Concentrationen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPotassium - Physiologyen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.subject.meshSuperoxide Dismutase - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshVasoconstrictor Agents - Antagonists & Inhibitorsen_US
dc.titlePotassium-induced release of endothelium-derived relaxing factor from 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.pmid3260148en_US
dc.identifier.scopuseid_2-s2.0-0023914997en_US
dc.identifier.volume62en_US
dc.identifier.issue6en_US
dc.identifier.spage1098en_US
dc.identifier.epage1103en_US
dc.identifier.isiWOS:A1988P049400007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRubanyi, GM=7005517991en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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