Albuminuria is an early marker of renovascular damage associated to an increase 
in oxidative stress. The Munich Wistar Frömter (MWF) rat is a model of chronic 
kidney disease (CKD), which exhibits endothelial dysfunction associated to low 
nitric oxide availability. We hypothesize that the new highly selective, 
non-steroidal mineralocorticoid receptor (MR) antagonist, finerenone, reverses 
both endothelial dysfunction and microalbuminuria. Twelve-week-old MWF (MWF-C; 
MWF-FIN) and aged-matched normoalbuminuric Wistar (W-C; W-FIN) rats were treated 
with finerenone (FIN, 10 mg/kg/day p.o.) or vehicle (C) for 4-week. Systolic 
blood pressure (SBP) and albuminuria were determined the last day of treatment. 
Finerenone lowered albuminuria by >40% and significantly reduced SBP in MWF. 
Aortic rings of MWF-C showed higher contractions to either noradrenaline (NA) or 
angiotensin II (Ang II), and lower relaxation to acetylcholine (Ach) than W-C 
rings. These alterations were reversed by finerenone to W-C control levels due 
to an upregulation in phosphorylated Akt and eNOS, and an increase in NO 
availability. Apocynin and 3-amino-1,2,4-triazole significantly reduced 
contractions to NA or Ang II in MWF-C, but not in MWF-FIN rings. Accordingly, a 
significant increase of Mn-superoxide dismutase (SOD) and Cu/Zn-SOD protein 
levels were observed in rings of MWF-FIN, without differences in p22phox, 
p47phox or catalase levels. Total SOD activity was increased in kidneys from 
MWF-FIN rats. In conclusion, finerenone improves endothelial dysfunction through 
an enhancement in NO bioavailability and a decrease in superoxide anion levels 
due to an upregulation in SOD activity. This is associated with an increase in 
renal SOD activity and a reduction of albuminuria.