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Time course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndrome
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2019 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 316, no 5, p. R563-R570Article in journal (Refereed) Published
Abstract [en]

The 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.

Place, publisher, year, edition, pages
the American Physiological Society , 2019. Vol. 316, no 5, p. R563-R570
Keywords [en]
animal model, congestive heart failure, pulmonary hypertension, right-sided heart failure
National Category
Physiology Cardiac and Cardiovascular Systems
Identifiers
URN: urn:nbn:se:umu:diva-159872DOI: 10.1152/ajpregu.00373.2018ISI: 000468436400001PubMedID: 30840486OAI: oai:DiVA.org:umu-159872DiVA, id: diva2:1322066
Funder
Åke Wiberg FoundationSwedish Heart Lung FoundationAvailable from: 2019-06-10 Created: 2019-06-10 Last updated: 2019-06-10Bibliographically approved

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Ericsson, MadeleneNilsson, Stefan K.

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Ericsson, MadeleneNilsson, Stefan K.Hultstrom, Michael
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American Journal of Physiology. Regulatory Integrative and Comparative Physiology
PhysiologyCardiac and Cardiovascular Systems

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