Background:

Sildenafil is a selective inhibitor of phosphodiesterase-5 (PDE5) [1].
Phosphodiesterases (PDEs) are enzymes that hydrolyzing cyclic nucleotides cAMP and cGMP to their inactive 5’-monofosfatos forms. The PDE5 enzyme is responsible for the hydrolysis of the cGMP, which restores GMP levels [1].
In human umbilical vein endothelial cells (HUVECs), Sildenafil (1 mM/5 h) significantly enhanced NO production, which is