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Article: Atrial natriuretic peptide decreases cardiac output independent of coronary vasoconstriction

TitleAtrial natriuretic peptide decreases cardiac output independent of coronary vasoconstriction
Authors
Issue Date1987
PublisherSociety for Experimental Biology and Medicine. The Journal's web site is located at http://www.ebmonline.org/
Citation
Proceedings Of The Society For Experimental Biology And Medicine, 1987, v. 186 n. 3, p. 313-318 How to Cite?
AbstractStudies were performed in isolated, Langendorff-perfused rat hearts and anesthetized dogs to determine the effects of synthetic atrial natriuretic peptide (ANP 8-33) on the coronary circulation. In vitro studies in the rat examined coronary flow dynamics to ANP 8-33 over a defined range from physiologic to pharmacologic concentrations. No changes in coronary flow or chronotropic and inotropic function of the isolated Langendorff-perfused heart were observed in response to increasing concentrations of ANP 8-33 (10 2 to 10 6 pg/ml). In the dog, a low, nonhypotensive dose of ANP 8-33 (0.05 μg/kg/min) decreased cardiac output with no change in coronary blood flow or coronary vascular resistance. At a high, hypotensive dose (0.3 μg/kg/min) ANP 8-33 decreased cardiac output in association with transient coronary vasodilation. Continued infusion resulted in a decrease in coronary blood flow and arterial pressure with no change in coronary vascular resistance. Thus, in vitro physiologic and pharmacologic concentrations of ANP, or in vivo low concentrations of ANP, do not result in an alteration in coronary flow. In vivo ANP 8-33, at both nonhypotensive and hypotensive concentrations, decreased cardiac output in the absence of coronary vasoconstriction.
Persistent Identifierhttp://hdl.handle.net/10722/170859
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBurnett Jr, JCen_US
dc.contributor.authorRubanyi, GMen_US
dc.contributor.authorEdwards, BSen_US
dc.contributor.authorSchwab, TRen_US
dc.contributor.authorZimmerman, RSen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:09Z-
dc.date.available2012-10-30T06:11:09Z-
dc.date.issued1987en_US
dc.identifier.citationProceedings Of The Society For Experimental Biology And Medicine, 1987, v. 186 n. 3, p. 313-318en_US
dc.identifier.issn0037-9727en_US
dc.identifier.urihttp://hdl.handle.net/10722/170859-
dc.description.abstractStudies were performed in isolated, Langendorff-perfused rat hearts and anesthetized dogs to determine the effects of synthetic atrial natriuretic peptide (ANP 8-33) on the coronary circulation. In vitro studies in the rat examined coronary flow dynamics to ANP 8-33 over a defined range from physiologic to pharmacologic concentrations. No changes in coronary flow or chronotropic and inotropic function of the isolated Langendorff-perfused heart were observed in response to increasing concentrations of ANP 8-33 (10 2 to 10 6 pg/ml). In the dog, a low, nonhypotensive dose of ANP 8-33 (0.05 μg/kg/min) decreased cardiac output with no change in coronary blood flow or coronary vascular resistance. At a high, hypotensive dose (0.3 μg/kg/min) ANP 8-33 decreased cardiac output in association with transient coronary vasodilation. Continued infusion resulted in a decrease in coronary blood flow and arterial pressure with no change in coronary vascular resistance. Thus, in vitro physiologic and pharmacologic concentrations of ANP, or in vivo low concentrations of ANP, do not result in an alteration in coronary flow. In vivo ANP 8-33, at both nonhypotensive and hypotensive concentrations, decreased cardiac output in the absence of coronary vasoconstriction.en_US
dc.languageengen_US
dc.publisherSociety for Experimental Biology and Medicine. The Journal's web site is located at http://www.ebmonline.org/en_US
dc.relation.ispartofProceedings of the Society for Experimental Biology and Medicineen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAtrial Natriuretic Factor - Pharmacologyen_US
dc.subject.meshBlood Pressure - Drug Effectsen_US
dc.subject.meshCardiac Output - Drug Effectsen_US
dc.subject.meshCoronary Circulation - Drug Effectsen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHeart Rate - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshPeptide Fragments - Pharmacologyen_US
dc.subject.meshPulmonary Wedge Pressure - Drug Effectsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshVascular Resistance - Drug Effectsen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleAtrial natriuretic peptide decreases cardiac output independent of coronary vasoconstrictionen_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.pmid2962199-
dc.identifier.scopuseid_2-s2.0-0023571372en_US
dc.identifier.volume186en_US
dc.identifier.issue3en_US
dc.identifier.spage313en_US
dc.identifier.epage318en_US
dc.identifier.isiWOS:A1987L541700010-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBurnett Jr, JC=35391042200en_US
dc.identifier.scopusauthoridRubanyi, GM=7005517991en_US
dc.identifier.scopusauthoridEdwards, BS=7202177472en_US
dc.identifier.scopusauthoridSchwab, TR=7003804590en_US
dc.identifier.scopusauthoridZimmerman, RS=7401650422en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl0037-9727-

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