Sildenafil is a potent inhibitor of phosphodiesterase 5 (PDE5) with IC₅₀ values of 3.6 and 3 nM for PDE5 activity in isolated rabbit platelets and human corpus cavernosum, respectively.¹ It is selective for PDE5 over PDE1 and PDE3 (IC₅₀s = 0.26 and 65 μM, respectively). Sildenafil reverses glucose-induced decreases in angiopoietin 1 (ANG1) expression and reduction of capillary-like tube formation by mouse dermal endothelial cells in vitro and increases the number of functional blood vessels and regional blood flow in the sciatic nerve in a db/db mouse model of diabetic peripheral neuropathy.² It increases the ratio of maximum intracavernosal pressure to mean arterial blood pressure (ICP/MAP), a measure of erectile function, in castrated rats when administered at a dose of 20 mg/kg per day.³ Sildenafil (0.5 mg/kg) also reduces cardiac arrest and resuscitation-induced increases in angiotensin II (Item No. 17150), angiotensin converting enzyme (ACE), ACE2, and various angiotensin receptors and increases survival in a porcine model of ischemia/reperfusion injury.⁴ Formulations containing sildenafil have been used in the treatment of erectile dysfunction, pulmonary arterial hypertension, and high-altitude pulmonary edema associated with altitude sickness.

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