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• W2091518393 abstract "Non-physiological activation of the mineralocorticoid receptor (MR), e.g. by aldosterone under conditions of high salt intake, contributes to the pathogenesis of cardiovascular diseases, although beneficial effects of aldosterone also have been described. The epidermal growth factor receptor (EGFR) contributes to cardiovascular alterations and mediates part of the MR effects. Recently, we showed that EGFR is required for physiological homeostasis and function of heart and arteries in adult animals. We hypothesize that moderate high aldosterone/NaCl, at normal blood pressure, affects the cardiovascular system depending on cardiovascular EGFR. Therefore we performed an experimental series in male and female animals each, using a recently established mouse model with EGFR knockout in vascular smooth muscle cells and cardiomyocytes and determined the effects of a mild-high aldosterone-to-NaCl constellation on a.o. marker gene expression, heart size, systolic blood pressure, impulse conduction and heart rate. Our data show that (i) cardiac tissue of male but not of female mice is sensitive to mild aldosterone/NaCl treatment, (ii) EGFR knockout induces stronger cardiac disturbances in male as compared to female animals and (iii) mild aldosterone/NaCl treatment requires the EGFR in order to disturb cardiac tissue homeostasis whereas beneficial effects of aldosterone seem to be independent of EGFR." @default.
• W2091518393 created "2016-06-24" @default.
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• W2091518393 date "2014-12-11" @default.
• W2091518393 modified "2023-10-03" @default.
• W2091518393 title "Moderate inappropriately high aldosterone/NaCl constellation in mice: cardiovascular effects and the role of cardiovascular epidermal growth factor receptor" @default.
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• W2091518393 doi "https://doi.org/10.1038/srep07430" @default.
• W2091518393 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4262830" @default.
• W2091518393 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25503263" @default.
• W2091518393 hasPublicationYear "2014" @default.
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