Hypothesis 2: Another new upraising strategy that has been used in attenuating renal injury in experimental studies is the use of phosphodiesterase type 5 (PDE5) inhibitor agents [77, 78]. PDE5 inhibitors are approved by the FDA for erectile dysfunction and pulmonary hypertension. The latter have been found to exert a significant antiapoptotic effect on renal tubular cells exposed to partial unilateral ureteral obstruction [79]. Part of the physiological process of PDE5 inhibition involves the release of nitric oxide (NO). Brando et al. linked the increase in available pool of cyclic 3,5 guanosine monophosphate (cGMP) by phosphodiesterases inhibitors to prevention and ameliorating chronic renal damage mainly by attenuating hypertension and retarding progression of renal disease [80]. Furthermore a PDE 5 inhibitor has been demonstrated to be able to ameliorate nephrotoxicity. Noami H. et al. have shown that FR226807, a selective PDE5 inhibitor, ameliorates cyclosporine A nephrotoxicity with further increases in cGMP content [81]. These observations may be of relevance for contrast media induced renal injury and suggest PDE5 inhibition as a potential therapeutic approach to this clinical entity.