Vardenafil

Mechanism

Vardenafil inhibits the cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum located around the penis. Penile erection during sexual stimulation is caused by increased penile blood flow resulting from the relaxation of penile arteries and corpus cavernosal smooth muscle. This response is mediated by the release of nitric oxide (NO) from nerve terminals and endothelial cells, which stimulates the synthesis of cGMP in smooth muscle cells. Cyclic GMP causes smooth muscle relaxation and increased blood flow into the corpus cavernosum. The inhibition of phosphodiesterase type 5 (PDE5) by vardenafil enhances erectile function by increasing the amount of cGMP.

Pharmacokinetics

• Absorption: Rapidly absorbed; peak plasma concentration reached within 30–120 minutes.
• Bioavailability: Approximately 15%; reduced with high‑fat meals.
• Distribution: Plasma protein binding ~95%; volume of distribution ~208 L.
• Metabolism: Extensively metabolized in the liver via CYP3A4 (major), CYP3A5 and CYP2C isoenzymes (minor).
• Excretion: Mainly via feces (~91–95%), small amount in urine (~2–6%).
• Half-life: Terminal elimination half-life ~4–5 hours.

Side Effects

• Headache
• Flushing
• Nasal congestion
• Dyspepsia
• Dizziness

Contraindication

• Use with nitrates
• Severe cardiovascular disorders
• Hypersensitivity to vardenafil

Interaction

• Nitrates: Severe hypotension risk
• CYP3A4 inhibitors: Increase vardenafil levels
• Alcohol: May enhance side effects

Warning and Precautions

• Use under medical supervision
• Caution in cardiovascular disease
• Avoid overdose

Dosage

As directed by the Physician.