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Article: Mechanisms of hypoxic vasoconstriction in the canine isolated pulmonary artery: Role of endothelium and sodium pump

TitleMechanisms of hypoxic vasoconstriction in the canine isolated pulmonary artery: Role of endothelium and sodium pump
Authors
Keywordshypoxia
prostanoids
Issue Date1994
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/
Citation
American Journal Of Physiology - Lung Cellular And Molecular Physiology, 1994, v. 267 n. 2 11-2, p. L120-L127 How to Cite?
AbstractContraction of canine pulmonary artery to hypoxia in vitro is both endothelium dependent and independent. The mechanisms which underlie this phenomenon were studied. Rings of canine pulmonary artery were suspended for isometric force recording in tissue baths containing modified Krebs-Ringer bicarbonate solution. Tissues were first contracted with norepinephrine [effective dose at 35% (ED35) concentration]. Subsequent exposure to hypoxia induced a triphasic response: an initial phasic transient contraction (phase 1), a transient reduction in force (phase 2), followed by a sustained tonic contraction (phase 3). In the absence of endothelium, all phases of the hypoxic response were reduced and phase 2 was reversed from a contraction to a relaxation (with endothelium: 0.68 ± 0.2 g; without endothelium: -0.34 ± 0.1 g). Similar data were obtained in the presence of nitro-L-arginine (3 x 10-5 M). In the absence of endothelium, indomethacin (10-5 M) abolished the phase 2 relaxation and converted phase 3 from a contraction to a relaxation (control: 0.99 ± 0.2 g; indomethacin: -0.44 ± 0.1 g); and ONO- 3708 (thromboxane A2/prostaglandin H2 receptor antagonist) diminished phase 3 (control: 0.99 ± 0.2 g; ONO-3708: 0.3 ± 0.04 g). In the absence of endothelium, but in the presence of indomethacin (10-5 M), K+-free solution diminished phase 1 (contraction) and converted phase 2 (relaxation) to a contraction (control: -0.74 ± 0.1 g; K+-free solution: 0.1 ± 0.06 g). Similar results were obtained with ouabain (4 x 10-7 M), and cooling of the bathing medium (20°C). The vascular endothelium, vasoactive prostanoids, and activity of the smooth muscle sodium pump may modulate the response to hypoxia in the canine isolated pulmonary artery.
Persistent Identifierhttp://hdl.handle.net/10722/171126
ISSN
2021 Impact Factor: 6.011
2020 SCImago Journal Rankings: 1.892
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHoshino, Yen_US
dc.contributor.authorMorrison, KJen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:18Z-
dc.date.available2012-10-30T06:12:18Z-
dc.date.issued1994en_US
dc.identifier.citationAmerican Journal Of Physiology - Lung Cellular And Molecular Physiology, 1994, v. 267 n. 2 11-2, p. L120-L127en_US
dc.identifier.issn1040-0605en_US
dc.identifier.urihttp://hdl.handle.net/10722/171126-
dc.description.abstractContraction of canine pulmonary artery to hypoxia in vitro is both endothelium dependent and independent. The mechanisms which underlie this phenomenon were studied. Rings of canine pulmonary artery were suspended for isometric force recording in tissue baths containing modified Krebs-Ringer bicarbonate solution. Tissues were first contracted with norepinephrine [effective dose at 35% (ED35) concentration]. Subsequent exposure to hypoxia induced a triphasic response: an initial phasic transient contraction (phase 1), a transient reduction in force (phase 2), followed by a sustained tonic contraction (phase 3). In the absence of endothelium, all phases of the hypoxic response were reduced and phase 2 was reversed from a contraction to a relaxation (with endothelium: 0.68 ± 0.2 g; without endothelium: -0.34 ± 0.1 g). Similar data were obtained in the presence of nitro-L-arginine (3 x 10-5 M). In the absence of endothelium, indomethacin (10-5 M) abolished the phase 2 relaxation and converted phase 3 from a contraction to a relaxation (control: 0.99 ± 0.2 g; indomethacin: -0.44 ± 0.1 g); and ONO- 3708 (thromboxane A2/prostaglandin H2 receptor antagonist) diminished phase 3 (control: 0.99 ± 0.2 g; ONO-3708: 0.3 ± 0.04 g). In the absence of endothelium, but in the presence of indomethacin (10-5 M), K+-free solution diminished phase 1 (contraction) and converted phase 2 (relaxation) to a contraction (control: -0.74 ± 0.1 g; K+-free solution: 0.1 ± 0.06 g). Similar results were obtained with ouabain (4 x 10-7 M), and cooling of the bathing medium (20°C). The vascular endothelium, vasoactive prostanoids, and activity of the smooth muscle sodium pump may modulate the response to hypoxia in the canine isolated pulmonary artery.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Lung Cellular and Molecular Physiologyen_US
dc.subjecthypoxia-
dc.subjectprostanoids-
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshOuabain - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshProstaglandins - Physiologyen_US
dc.subject.meshPulmonary Artery - Drug Effects - Physiopathologyen_US
dc.subject.meshSodium-Potassium-Exchanging Atpase - Physiologyen_US
dc.subject.meshVasoconstrictionen_US
dc.titleMechanisms of hypoxic vasoconstriction in the canine isolated pulmonary artery: Role of endothelium and sodium pumpen_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.pmid8074234-
dc.identifier.scopuseid_2-s2.0-0028124404en_US
dc.identifier.volume267en_US
dc.identifier.issue2 11-2en_US
dc.identifier.spageL120en_US
dc.identifier.epageL127en_US
dc.identifier.isiWOS:A1994PC43900085-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHoshino, Y=7202851283en_US
dc.identifier.scopusauthoridMorrison, KJ=7102484828en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl1040-0605-

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