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Time course of deco...
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Becirovic-Agic, MedihaUppsala universitet,Integrativ Fysiologi
(författare)
Time course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndrome
- Artikel/kapitelEngelska2019
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the American Physiological Society,2019
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printrdacarrier
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LIBRIS-ID:oai:DiVA.org:umu-159872
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-159872URI
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https://doi.org/10.1152/ajpregu.00373.2018DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-380656URI
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Språk:engelska
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Sammanfattning på:engelska
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Title in thesis list of papers: 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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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.
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Jönsson, SofiaUppsala universitet,Integrativ Fysiologi(Swepub:uu)sofjo523
(författare)
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Tveitarås, Maria K.
(författare)
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Skogstrand, Trude
(författare)
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Karlsen, Tine, V
(författare)
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Lidén, Åsa
(författare)
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Leh, Sabine
(författare)
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Ericsson, MadeleneUmeå universitet,Fysiologisk kemi(Swepub:umu)maer0239
(författare)
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Nilsson, Stefan K.,1979-Umeå universitet,Fysiologisk kemi(Swepub:umu)nist6501
(författare)
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Reed, Rolf K.
(författare)
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Hultström, Michael,1978-Uppsala universitet,Anestesiologi och intensivvård,Integrativ Fysiologi,Department of Biomedicine, University of Bergen, Bergen, Norway(Swepub:uu)mihul498
(författare)
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Uppsala universitetIntegrativ Fysiologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:American Journal of Physiology. Regulatory Integrative and Comparative Physiology: the American Physiological Society316:5, s. R563-R5700363-61191522-1490
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Lidén, Åsa
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Leh, Sabine
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Reed, Rolf K.
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