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Nitric Oxide (NO) acts as a vasodilator in the process of penile erection. NO is supplied from two sources. The first is as a neurotransmitter liberated by the cavernous nerve which innervates smooth muscle surrounding penile arteries. The second source is the endothelial cells lining the deep arteries of the penis. Endothelium-derived NO is formed in response to stimulation of the endothelial cells by cholinergic nerves. Acetylcholine causes the production of inositol triphosphate (IP3), an important second messenger in many hormone signal transduction pathways. IP3 opens calcium channels in the endoplasmic membrane of the endothelial cells; the liberated calcium then activates NO synthase and causes the production of NO.
As a gas, NO is able to pass through cell membranes without the aid of dedicated transporters and its free radical character makes it particularly reactive with iron-containing proteins.
Whatever the source, endothelial cells or cavernous nerve, NO diffuses across the muscle cell membrane and binds to guanylyl cyclase. Guanylyl cyclase catalyzes the synthesis of cyclic GMP from GTP. cGMP then activates a cGMP dependent protein kinase which in turn stimulates the uptake of calcium by the endoplasmic reticulum of the muscle cell. The reduced levels of cytoplasmic calcium cause the muscle cell to relax. As a consequence of muscle cell relaxation, vasodilation occurs.
