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Article: Adenosine elicits an eNOS-independent reduction in arterial blood pressure in conscious mice that involves adenosine A 2A receptors

TitleAdenosine elicits an eNOS-independent reduction in arterial blood pressure in conscious mice that involves adenosine A 2A receptors
Authors
Issue Date2011
PublisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1748-1708
Citation
Acta Physiologica, 2011, v. 203 n. 1, p. 197-207 How to Cite?
AbstractAims: Adenosine plays an important role in the regulation of heart rate (HR) and vascular reactivity. However, the mechanisms underlying the acute effect of adenosine on arterial blood pressure in conscious mice are unclear. Therefore, this study investigated the effect of the nucleoside on mean arterial blood pressure (MAP) and HR in conscious mice. Methods: Chronic indwelling catheters were placed in C57Bl/6J (WT) and endothelial nitric oxide synthase knockout (eNOS -/-) mice for continuous measurements of MAP and HR. Using PCR and myograph analysis, involvement of adenosine receptors was investigated in human and mouse renal blood vessels. Results: Bolus infusion of 0.5mgkg -1 adenosine elicited significant transient decreases in MAP (99.3±2.3 to 70.4±4.5mmHg) and HR (603.2±18.3 to 364.3±49.2min -1), which were inhibited by the A 2A receptor antagonist ZM 241385. Activation of adenosine A 2A receptors with CGS 21680 (0.02mgkg -1) caused a significant reduction in MAP from 99.6±1.2 to 73.1±3.6mmHg accompanied by tachycardia (610.5±9.3 to 677.5±9.5min -1). The reduction in MAP observed after adenosine or CGS 21680 administrations was not significantly different in WT and eNOS -/- mice. In isolated human and mouse intrarenal arteries, adenosine caused a relaxation dependent on A 2A adenosine receptor activation. A 2A receptors were present in both human and mouse arteries whereas A 1 and A 2B receptors were only present in mouse arteries. Conclusion: In conclusion, acute adenosine administration and selective stimulation of adenosine A 2A receptors results in an immediate, transient eNOS-independent reduction in MAP. A 2A receptor activation causes relaxation of human and mouse arteries. © 2010 The Authors. Acta Physiologica © 2010 Scandinavian Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/171428
ISSN
2015 Impact Factor: 4.066
2015 SCImago Journal Rankings: 1.690
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAndersen, Hen_US
dc.contributor.authorJaff, MGen_US
dc.contributor.authorHøgh, Den_US
dc.contributor.authorVanhoutte, Pen_US
dc.contributor.authorHansen, PBen_US
dc.date.accessioned2012-10-30T06:14:07Z-
dc.date.available2012-10-30T06:14:07Z-
dc.date.issued2011en_US
dc.identifier.citationActa Physiologica, 2011, v. 203 n. 1, p. 197-207en_US
dc.identifier.issn1748-1708en_US
dc.identifier.urihttp://hdl.handle.net/10722/171428-
dc.description.abstractAims: Adenosine plays an important role in the regulation of heart rate (HR) and vascular reactivity. However, the mechanisms underlying the acute effect of adenosine on arterial blood pressure in conscious mice are unclear. Therefore, this study investigated the effect of the nucleoside on mean arterial blood pressure (MAP) and HR in conscious mice. Methods: Chronic indwelling catheters were placed in C57Bl/6J (WT) and endothelial nitric oxide synthase knockout (eNOS -/-) mice for continuous measurements of MAP and HR. Using PCR and myograph analysis, involvement of adenosine receptors was investigated in human and mouse renal blood vessels. Results: Bolus infusion of 0.5mgkg -1 adenosine elicited significant transient decreases in MAP (99.3±2.3 to 70.4±4.5mmHg) and HR (603.2±18.3 to 364.3±49.2min -1), which were inhibited by the A 2A receptor antagonist ZM 241385. Activation of adenosine A 2A receptors with CGS 21680 (0.02mgkg -1) caused a significant reduction in MAP from 99.6±1.2 to 73.1±3.6mmHg accompanied by tachycardia (610.5±9.3 to 677.5±9.5min -1). The reduction in MAP observed after adenosine or CGS 21680 administrations was not significantly different in WT and eNOS -/- mice. In isolated human and mouse intrarenal arteries, adenosine caused a relaxation dependent on A 2A adenosine receptor activation. A 2A receptors were present in both human and mouse arteries whereas A 1 and A 2B receptors were only present in mouse arteries. Conclusion: In conclusion, acute adenosine administration and selective stimulation of adenosine A 2A receptors results in an immediate, transient eNOS-independent reduction in MAP. A 2A receptor activation causes relaxation of human and mouse arteries. © 2010 The Authors. Acta Physiologica © 2010 Scandinavian Physiological Society.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1748-1708en_US
dc.relation.ispartofActa Physiologicaen_US
dc.subject.meshAdenosine - Metabolism - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Pressure - Drug Effects - Physiologyen_US
dc.subject.meshConsciousnessen_US
dc.subject.meshFemaleen_US
dc.subject.meshHeart Rate - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshNitric Oxide Synthase Type Iii - Metabolismen_US
dc.subject.meshReceptor, Adenosine A2a - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.titleAdenosine elicits an eNOS-independent reduction in arterial blood pressure in conscious mice that involves adenosine A 2A receptorsen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, P:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, P=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1748-1716.2010.02218.xen_US
dc.identifier.pmid21062422-
dc.identifier.scopuseid_2-s2.0-80051613644en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80051613644&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume203en_US
dc.identifier.issue1en_US
dc.identifier.spage197en_US
dc.identifier.epage207en_US
dc.identifier.isiWOS:000293921400018-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridAndersen, H=7402273048en_US
dc.identifier.scopusauthoridJaff, MG=49661606900en_US
dc.identifier.scopusauthoridHøgh, D=49661306200en_US
dc.identifier.scopusauthoridVanhoutte, P=7202304247en_US
dc.identifier.scopusauthoridHansen, PB=35472646600en_US
dc.identifier.citeulike9714492-

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