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Article: Continuous flow augments reactivity of rabbit carotid artery by reducing bioavailability of NO despite an increase in release of EDHF

TitleContinuous flow augments reactivity of rabbit carotid artery by reducing bioavailability of NO despite an increase in release of EDHF
Authors
Issue Date2006
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2006, v. 291 n. 4, p. H1521-H1528 How to Cite?
AbstractExperiments were designed to investigate the influence of steady flow and pressure on endothelial function in the rabbit carotid artery. Increases and decreases in isometric force were compared in static rings and perfused (5 or 50 ml/min) segments of the same arteries in the presence and absence of endothelium. The α1-adrenoceptor agonist phenylephrine and the muscarinic agonist acetylcholine were applied as vasoconstrictor and vasodilator stimuli, respectively. Continuous flow (5 and 50 ml/min) reduced the cGMP content and shifted the concentration-response curve to phenylephrine to the left compared with nonperfused static rings. Removal of the endothelium abolished the differences in cGMP content and the sensitivity to phenylephrine between static rings and perfused segments. No difference in sensitivity to phenylephrine was observed in tissues treated with Nω-nitro-L- arginine methyl ester (L-NAME). Acetylcholine-evoked relaxations were increased in perfused segments. L-NAME nearly abolished the acetylcholine-evoked relaxation in static rings, whereas about one-half of the relaxation remained in segments exposed to flow. This remnant relaxation was blocked by inhibition of endothelial small- and intermediate-conductance calcium-activated potassium channels by apamin plus 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34). These experiments demonstrate that continuous flow increases the constriction evoked by α1-adrenergic activation in the rabbit carotid artery through a reduced influence of basally released endothelial NO and, furthermore, that luminal flow unmasks an ability of the endothelium to release a non-NO, noncyclooxygenase vasodilator, presumably endothelium-derived hyperpolarizing factor. Copyright © 2006 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/171347
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRasmussen, LEen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorJensen, BLen_US
dc.contributor.authorSkøtt, Oen_US
dc.date.accessioned2012-10-30T06:13:31Z-
dc.date.available2012-10-30T06:13:31Z-
dc.date.issued2006en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2006, v. 291 n. 4, p. H1521-H1528en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/171347-
dc.description.abstractExperiments were designed to investigate the influence of steady flow and pressure on endothelial function in the rabbit carotid artery. Increases and decreases in isometric force were compared in static rings and perfused (5 or 50 ml/min) segments of the same arteries in the presence and absence of endothelium. The α1-adrenoceptor agonist phenylephrine and the muscarinic agonist acetylcholine were applied as vasoconstrictor and vasodilator stimuli, respectively. Continuous flow (5 and 50 ml/min) reduced the cGMP content and shifted the concentration-response curve to phenylephrine to the left compared with nonperfused static rings. Removal of the endothelium abolished the differences in cGMP content and the sensitivity to phenylephrine between static rings and perfused segments. No difference in sensitivity to phenylephrine was observed in tissues treated with Nω-nitro-L- arginine methyl ester (L-NAME). Acetylcholine-evoked relaxations were increased in perfused segments. L-NAME nearly abolished the acetylcholine-evoked relaxation in static rings, whereas about one-half of the relaxation remained in segments exposed to flow. This remnant relaxation was blocked by inhibition of endothelial small- and intermediate-conductance calcium-activated potassium channels by apamin plus 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34). These experiments demonstrate that continuous flow increases the constriction evoked by α1-adrenergic activation in the rabbit carotid artery through a reduced influence of basally released endothelial NO and, furthermore, that luminal flow unmasks an ability of the endothelium to release a non-NO, noncyclooxygenase vasodilator, presumably endothelium-derived hyperpolarizing factor. Copyright © 2006 the American Physiological Society.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Metabolismen_US
dc.subject.meshCarotid Arteries - Physiologyen_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshCyclooxygenase Inhibitors - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshEpoprostenol - Metabolismen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshNg-Nitroarginine Methyl Ester - Pharmacologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshPyrazoles - Pharmacologyen_US
dc.subject.meshRabbitsen_US
dc.subject.meshRegional Blood Flow - Physiologyen_US
dc.subject.meshVasoconstriction - Drug Effects - Physiologyen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleContinuous flow augments reactivity of rabbit carotid artery by reducing bioavailability of NO despite an increase in release of EDHFen_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.doi10.1152/ajpheart.00027.2006en_US
dc.identifier.pmid16648195-
dc.identifier.scopuseid_2-s2.0-33749331623en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33749331623&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume291en_US
dc.identifier.issue4en_US
dc.identifier.spageH1521en_US
dc.identifier.epageH1528en_US
dc.identifier.isiWOS:000240509700004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRasmussen, LE=7201874847en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridJensen, BL=35502338900en_US
dc.identifier.scopusauthoridSkøtt, O=7005724990en_US

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