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dc.contributor.authorBecirovic-Agic, Medihaen_US
dc.contributor.authorJönsson, Sofiaen_US
dc.contributor.authorTveitarås, Maria Kathrineen_US
dc.contributor.authorSkogstrand, Trudeen_US
dc.contributor.authorKarlsen, Tine Veronicaen_US
dc.contributor.authorLiden, Åsaen_US
dc.contributor.authorLeh, Sabine Mariaen_US
dc.contributor.authorEricsson, Madeleneen_US
dc.contributor.authorNilsson, Stefan K.en_US
dc.contributor.authorReed, Rolf K.en_US
dc.contributor.authorHultström, Michaelen_US
dc.date.accessioned2020-04-21T11:33:42Z
dc.date.available2020-04-21T11:33:42Z
dc.date.issued2019-05-01
dc.PublishedBecirovic-Agic, Jönsson S, Tveitarås MK, Skogstrand T, Karlsen TV, Liden Å, Leh S, Ericsson ME, Nilsson SK, Reed RK, Hultström M. Time course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndrome. American Journal of Physiology. Regulatory Integrative and Comparative Physiology. 2019;316(5):R563-R570.eng
dc.identifier.issn1522-1490
dc.identifier.issn0363-6119
dc.identifier.urihttps://hdl.handle.net/1956/21954
dc.description.abstractThe genetic background of a mouse strain determines its susceptibility to disease. C57BL/6J and Balb/CJ are two widely used inbred mouse strains that we found react dramatically differently to angiotensin II and high-salt diet (ANG II + Salt). Balb/CJ show increased mortality associated with anuria and edema formation while C57BL/6J develop arterial hypertension but do not decompensate and die. Clinical symptoms of heart failure in Balb/CJ mice gave the hypothesis that ANG II + Salt impairs cardiac function and induces cardiac remodeling in male Balb/CJ but not in male C57BL/6J mice. To test this hypothesis, we measured cardiac function using echocardiography before treatment and every day for 7 days during treatment with ANG II + Salt. Interestingly, pulsed wave Doppler of pulmonary artery flow indicated increased pulmonary vascular resistance and right ventricle systolic pressure in Balb/CJ mice, already 24 h after ANG II + Salt treatment was started. In addition, Balb/CJ mice showed abnormal diastolic filling indicated by reduced early and late filling and increased isovolumic relaxation time. Furthermore, Balb/CJ exhibited lower cardiac output compared with C57BL/6J even though they retained more sodium and water, as assessed using metabolic cages. Left posterior wall thickness increased during ANG II + Salt treatment but did not differ between the strains. In conclusion, ANG II + Salt treatment causes early restriction of pulmonary flow and reduced left ventricular filling and cardiac output in Balb/CJ, which results in fluid retention and peripheral edema. This makes Balb/CJ a potential model to study the adaptive capacity of the heart for identifying new disease mechanisms and drug targets.en_US
dc.language.isoengeng
dc.publisherAmerican Physiological Societyeng
dc.subjectanimal modeleng
dc.subjectcongestive heart failureeng
dc.subjectpulmonary hypertensioneng
dc.subjectright-sided heart failureeng
dc.titleTime course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndromeen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2020-02-03T12:49:27Z
dc.description.versionacceptedVersionen_US
dc.rights.holderCopyright 2019 the American Physiological Society
dc.identifier.doihttps://doi.org/10.1152/ajpregu.00373.2018
dc.identifier.cristin1709325
dc.source.journalAmerican Journal of Physiology. Regulatory Integrative and Comparative Physiology
dc.source.pagenumberR563-R570
dc.identifier.citationAmerican Journal of Physiology. Regulatory Integrative and Comparative Physiology. 2019;316(5):R563-R570.
dc.source.volume316
dc.source.issue5


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