The mechanism of action of Sildenafil (Viagra) is one of enzyme kinetics. In the lumen of blood vessels are endothelial cells. Acyteylcholine binds to a 7-transmembrane protein receptor, activating the Phospholipase C pathway. Phospholipase C splits a molecule of Innositol Triphosphate into Diacyl glycerol and IP3. IP3 goes into the endoplasmic reticulum to release stores of Calcium Ion channels. The increased Calcium bumbs into a protein called Calmodulin, which when activated activates Nitric Oxide synthase. Nitric Oxide synthase catalyzes the formation of Nitric Oxide (NO), which leaves the endothelial cell lining the walls of blood vessels into near by smooth muscle cells lining the outer wall of the blood vessel. The receptor of the NO is also an anzyme, that catalyzes the formation of Cyclic GMP (cGMP). Now cGMP activates protein kinase G (PKG), whose ultimate outcome is the dissociation of the actin-myosin complex of smooth muscle cells leading to increased smooth muscle relaxation. Normally the cGMP formed is hydrolyzed by a cGMP phosphodiesterase.
All that Viagra does, is to prolong the half life of the cGMP molecule, so that it can activate more PKG, which leads to more smooth muslce relaxation of blood vessel walls leading to greater blood flow to ischiocavernosus muscles of the penis and hence greater erection time.
Sildenafil has greater affinity for PDE-5, a type of phosphodiesterase found in the smooth muscle walls of erectile tissue.