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Cardiac structure and function in a mouse model of uraemia without hypertension

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Cardiac structure and function in a mouse model of uraemia without hypertension. / Bro, Susanne; Bollano, Entela; Bruel, Annemarie; Olgaard, Klaus; Nielsen, Lars.

I: Scandinavian Journal of Clinical & Laboratory Investigation, 2008, s. 1-7.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Bro, S, Bollano, E, Bruel, A, Olgaard, K & Nielsen, L 2008, 'Cardiac structure and function in a mouse model of uraemia without hypertension', Scandinavian Journal of Clinical & Laboratory Investigation, s. 1-7. https://doi.org/10.1080/00365510802037272

APA

Bro, S., Bollano, E., Bruel, A., Olgaard, K., & Nielsen, L. (2008). Cardiac structure and function in a mouse model of uraemia without hypertension. Scandinavian Journal of Clinical & Laboratory Investigation, 1-7. https://doi.org/10.1080/00365510802037272

CBE

Bro S, Bollano E, Bruel A, Olgaard K, Nielsen L. 2008. Cardiac structure and function in a mouse model of uraemia without hypertension. Scandinavian Journal of Clinical & Laboratory Investigation. 1-7. https://doi.org/10.1080/00365510802037272

MLA

Bro, Susanne o.a.. "Cardiac structure and function in a mouse model of uraemia without hypertension". Scandinavian Journal of Clinical & Laboratory Investigation. 2008, 1-7. https://doi.org/10.1080/00365510802037272

Vancouver

Bro S, Bollano E, Bruel A, Olgaard K, Nielsen L. Cardiac structure and function in a mouse model of uraemia without hypertension. Scandinavian Journal of Clinical & Laboratory Investigation. 2008;1-7. https://doi.org/10.1080/00365510802037272

Author

Bro, Susanne ; Bollano, Entela ; Bruel, Annemarie ; Olgaard, Klaus ; Nielsen, Lars. / Cardiac structure and function in a mouse model of uraemia without hypertension. I: Scandinavian Journal of Clinical & Laboratory Investigation. 2008 ; s. 1-7.

Bibtex

@article{a5366e70ca8211dd9710000ea68e967b,
title = "Cardiac structure and function in a mouse model of uraemia without hypertension",
abstract = "Kidney dysfunction is often associated with cardiac left ventricular hypertrophy and increased cardiovascular mortality. Objective. The aim of this study was to find out whether this reflects direct effects of uraemia on the heart or is dependent on accompanying hypertension. Material and methods. Apolipoprotein-E (apoE)-deficient C57BL/6 mice are resistant to development of hypertension after renal mass reduction. To evaluate the impact of uraemia without hypertension on the heart, apoE-deficient mice underwent 5/6 nephrectomy (NX) or sham operation (Sh) and were randomized to treatment with the angiotensin converting enzyme inhibitor enalapril (12 mg kg(-1) d(-1)) or no medication. Results. NX did not affect systolic blood pressure (BP), but reduced mean creatinine clearance, body weight and blood haemoglobin to 27 % (p<0.01), 82 % (p<0.0001) and 73 % (p<0.0001), respectively, of the values in Sh mice. Thirty-six weeks after NX, heart wet weight, echocardiographic estimates of left ventricular mass and left ventricular diastolic and systolic functions were similar in NX and Sh mice. NX did not increase cardiac fibrosis or cardiac mRNA expression of biglycan, whereas it decreased the mRNA expression of procollagen (p<0.01). Enalapril reduced BP (p<0.001), heart wet weight and estimated left ventricular mass in both NX (p<0.01) and Sh mice (p<0.05), but did not affect cardiac diastolic or systolic function. Conclusions. The results suggest that uraemia does not impair cardiac structure or function in apoE-deficient mice. Since NX has no effect on BP in apoE-deficient mice, the results may indicate that hypertension is important for development of left ventricular disease in uraemia.",
author = "Susanne Bro and Entela Bollano and Annemarie Bruel and Klaus Olgaard and Lars Nielsen",
year = "2008",
doi = "10.1080/00365510802037272",
language = "English",
pages = "1--7",
journal = "Scandinavian Journal of Clinical & Laboratory Investigation",
issn = "0036-5513",
publisher = "Taylor & Francis ",

}

RIS

TY - JOUR

T1 - Cardiac structure and function in a mouse model of uraemia without hypertension

AU - Bro, Susanne

AU - Bollano, Entela

AU - Bruel, Annemarie

AU - Olgaard, Klaus

AU - Nielsen, Lars

PY - 2008

Y1 - 2008

N2 - Kidney dysfunction is often associated with cardiac left ventricular hypertrophy and increased cardiovascular mortality. Objective. The aim of this study was to find out whether this reflects direct effects of uraemia on the heart or is dependent on accompanying hypertension. Material and methods. Apolipoprotein-E (apoE)-deficient C57BL/6 mice are resistant to development of hypertension after renal mass reduction. To evaluate the impact of uraemia without hypertension on the heart, apoE-deficient mice underwent 5/6 nephrectomy (NX) or sham operation (Sh) and were randomized to treatment with the angiotensin converting enzyme inhibitor enalapril (12 mg kg(-1) d(-1)) or no medication. Results. NX did not affect systolic blood pressure (BP), but reduced mean creatinine clearance, body weight and blood haemoglobin to 27 % (p<0.01), 82 % (p<0.0001) and 73 % (p<0.0001), respectively, of the values in Sh mice. Thirty-six weeks after NX, heart wet weight, echocardiographic estimates of left ventricular mass and left ventricular diastolic and systolic functions were similar in NX and Sh mice. NX did not increase cardiac fibrosis or cardiac mRNA expression of biglycan, whereas it decreased the mRNA expression of procollagen (p<0.01). Enalapril reduced BP (p<0.001), heart wet weight and estimated left ventricular mass in both NX (p<0.01) and Sh mice (p<0.05), but did not affect cardiac diastolic or systolic function. Conclusions. The results suggest that uraemia does not impair cardiac structure or function in apoE-deficient mice. Since NX has no effect on BP in apoE-deficient mice, the results may indicate that hypertension is important for development of left ventricular disease in uraemia.

AB - Kidney dysfunction is often associated with cardiac left ventricular hypertrophy and increased cardiovascular mortality. Objective. The aim of this study was to find out whether this reflects direct effects of uraemia on the heart or is dependent on accompanying hypertension. Material and methods. Apolipoprotein-E (apoE)-deficient C57BL/6 mice are resistant to development of hypertension after renal mass reduction. To evaluate the impact of uraemia without hypertension on the heart, apoE-deficient mice underwent 5/6 nephrectomy (NX) or sham operation (Sh) and were randomized to treatment with the angiotensin converting enzyme inhibitor enalapril (12 mg kg(-1) d(-1)) or no medication. Results. NX did not affect systolic blood pressure (BP), but reduced mean creatinine clearance, body weight and blood haemoglobin to 27 % (p<0.01), 82 % (p<0.0001) and 73 % (p<0.0001), respectively, of the values in Sh mice. Thirty-six weeks after NX, heart wet weight, echocardiographic estimates of left ventricular mass and left ventricular diastolic and systolic functions were similar in NX and Sh mice. NX did not increase cardiac fibrosis or cardiac mRNA expression of biglycan, whereas it decreased the mRNA expression of procollagen (p<0.01). Enalapril reduced BP (p<0.001), heart wet weight and estimated left ventricular mass in both NX (p<0.01) and Sh mice (p<0.05), but did not affect cardiac diastolic or systolic function. Conclusions. The results suggest that uraemia does not impair cardiac structure or function in apoE-deficient mice. Since NX has no effect on BP in apoE-deficient mice, the results may indicate that hypertension is important for development of left ventricular disease in uraemia.

U2 - 10.1080/00365510802037272

DO - 10.1080/00365510802037272

M3 - Journal article

C2 - 18609109

SP - 1

EP - 7

JO - Scandinavian Journal of Clinical & Laboratory Investigation

JF - Scandinavian Journal of Clinical & Laboratory Investigation

SN - 0036-5513

ER -