Key result
Aldosterone induced glomerular damage, increased systolic blood pressure, and increased albumin permeability, effects that were worsened by salt and reduced by eplerenone.
Why the study?
Does aldosterone, alone or with salt, cause glomerular structural and functional damage in uninephrectomized rats?
Does aldosterone, alone or with salt, cause glomerular structural and functional damage in uninephrectomized rats?
Aldosterone induces glomerular structural and functional damage, which is exacerbated by salt and mitigated by eplerenone, potentially via ACE/ACE2 dysregulation.
Hypothesis-generating for eplerenone in salt-sensitive glomerular disease; human trials needed before clinical consideration.
OBJECTIVE: Experimental evidence suggests that aldosterone directly contributes to organ damage by promoting cell growth, fibrosis, and inflammation. Based on these premises, this work aimed to assess the glomerular effects of aldosterone, alone and in combination with salt. METHODS: After undergoing uninephrectomy, 75 rats were allocated to five groups: control, salt diet, aldosterone, aldosterone + salt diet, aldosterone + salt diet and eplerenone, and they were all studied for four weeks. We focused on glomerular structural, functional, and molecular changes, including slit diaphragm components, local renin-angiotensin system activation, as well as pro-oxidative and profibrotic changes. RESULTS: Aldosterone significantly increased systolic blood pressure, led to glomerular hypertrophy, mesangial expansion, and it significantly increased the glomerular permeability to albumin and the albumin excretion rate, indicating the presence of glomerular damage. These effects were worsened by adding salt to aldosterone, while they were reduced by eplerenone. Aldosterone-induced glomerular damage was associated with glomerular angiotensin-converting enzyme (ACE) 2 downregulation, with ACE/ACE2 ratio increase, ANP decrease, as well as with glomerular pro-oxidative and profibrotic changes. CONCLUSIONS: Aldosterone damages not only the structure but also the function of the glomerulus. ACE/ACE2 upregulation, ACE2 and ANP downregulation, and pro-oxidative and profibrotic changes are possible mechanisms accounting for aldosterone-induced glomerular injury.
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Bernardi et al. (2015) studied Glomerular damage (n=75). Aldosterone vs. Control, salt diet, or aldosterone + salt + eplerenone was evaluated on Glomerular structural, functional, and molecular changes. Aldosterone induced glomerular damage, increased systolic blood pressure, and increased albumin permeability, effects that were worsened by salt and reduced by eplerenone.
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