Aldosterone Antagonism Improves Endothelial-Dependent Vasorelaxation in Heart Failure via Upregulation of Endothelial Nitric Oxide Synthase Production

Spironolactone prevents the decrease in eNOS in the LV and aorta and improves NO-dependent vasorelaxation, suggesting that one potential mechanism of spironolactone is an improvement in vasoreactivity mediated though an increase in NO.