If viewed in cross section, the glans of the penis reveal that the penis consists of three tube-like projections of spongy tissue, the corpus spongiosum, located ventrally and the paired corpi cavernosi located dorsally. In each of the latter is the deep artery of the penis which carries blood over the length of the penis into the open channels that make up the corpus cavernosum. The blood carried out of the corpi cavernosi empties into the dorsal vein of the penis which then returns the blood to the body. It is thought that the level of rigidity of the penis is due to the relationship between arterial inflow and venous outflow in the penis. This means that the larger the calibre of the arteries, the more blood enters the corpus cavernosum and enlarges the penis, and the larger the calibre of the veins, the more blood is shunted away from the penis. An erection is an involuntary action controlled by the autonomic nervous system which consists of the sympathetic and parasympathetic pathways. In general, sympathetic stimulation leads to the constriction of smooth muscle surrounding the arteries (reducing the calibre) and parasympathetic stimulation induces smooth muscle relaxation (larger artery). When stimulated sexually, the sympathetic stimulation of the penis decreases and the parasympathetic stimulation increases. It is the terminal of the axons of the parasympathetic nerves that release NO. The mechanism that causes erection is then the one shown above. The engorged sinusoids of the corpi cavernosi compress the penile veins, which reduces blood outflow from the penis. Blood is therefore trapped in the penis, which maintains the erection.
The cycle of transformations of guanosine triphosphate is shown in more detail below (GC-Guanosine cyclase):
PKG can also have other effects in cells, for example by activating a number of transcription factors which can lead to changes in gene expression which in turn can alter the response of the cell to a variety of stimuli.
Once produced cGMP can have a number of effects in cells, but many of those effects are mediated through the activation of protein kinase G (PKG). Active PKG is ultimately responsible for many of the effects of Nitric Oxide including its effects on blood vessel relaxation (vasodilation). Activation of PKG by cGMP leads to activation of myosin phosphatase which in turn leads to release of calcium from intracellular stores in smooth muscle cells. This in turn leads to relaxation of the smooth muscle cells. In the case of vasodilation the Nitric Oxide is originally produced in the neighbouring endothelial cells before diffusing into the smooth muscle cells where it actiavtes sGC and cGMP production.
As you might expect, cGMP is not infinitely stable; otherwise a man might have an erection forever. cGMP is removed by the action of cGMP phosphodiesterase, which converts it to GMP. The turnover of cGMP in the penis is quite rapid leading to lack of signal unless NO is continually produced by the NANC nerve cells in order to replenish the supply of cGMP by reactivating guanylyl cyclase. This production of NO requires the attention of the brain, which has to keep focused on the task at hand.
Nitric oxide acts locally. It diffuses into adjacent cells and binds to an enzyme called guanylyl cyclase. The binding of NO activates the enzyme, stimulating it to produce cyclic guanosine monophosphate or cGMP. The substrate for this reaction is guanosine triphosphate (GTP), a molecule that's similar to ATP except that the base is guanine instead of adenine.
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