Key result
Aldosterone/NaCl treatment increases 28-day mortality by ~46 percentage points in EGFR-knockout mice.
Why the study?
The epidermal growth factor receptor (EGFR) mediates part of the mineralocorticoid receptor effects and is required for cardiovascular homeostasis in adult animals. This study tested the hypothesis that moderately high aldosterone/NaCl at normal blood pressure affects the cardiovascular system depending on cardiovascular EGFR.
Answers are grounded in this paper and cite their sources.
Preclinical mouse data do not alter clinical aldosterone use; extends evidence for sex-specific, EGFR-dependent cardiac effects but leaves human translation open.
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.
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Schreier et al. (2014) studied Cardiovascular alterations induced by moderate high aldosterone/NaCl intake (n=72). Aldosterone and NaCl vs. Untreated control across wildtype and EGFR-knockout genotypes was evaluated on 28-day mortality and cardiac tissue homeostasis (hypertrophy, conduction, and fibrotic marker gene expression) (p=<0.05). Mild aldosterone/NaCl treatment increased 28-day mortality by 45.5% in male EGFR-knockout mice and induced EGFR-dependent cardiac fibrosis markers and PR-prolongation in male wildtype mice.
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