Mechanisms of erection

Intracavernosal smooth muscle tone is by far the most important determinant of intracavernosal blood flow. Approximately half of the cavernosal volume is composed of smooth muscle, with the remainder consisting of either lacunar spaces or collagen. Collagen fibers are largely responsible for the passive mechanical properties of cavernosal tissue. In contrast, active contraction of cavernosal smooth muscle is dependent upon a number of factors, including the level of agonists (neurotransmitters, hormones and endothelium-derived factors), adequate expression of receptors, integrity of transduction mechanisms, calcium homeostasis, interaction of contractile proteins, and intimate intracellular communication between smooth muscle cells (gap junctions).

Cavernosal smooth muscle cells contain abundant amounts of the contractile proteins, actin and myosin. Following phosphorylation of myosin by adenosine triphosphate (ATP), attachments (crossbridges) form between the light chains of these two proteins and these attachments provide the mechanism for contractile tone of smooth muscle. The expenditure of energy for maintaining this state of tone is almost zero, but there is an absolute requirement for a high concentration of cytoplasmic free calcium.

Adequate calcium homeostasis is, therefore, fundamental to the normal regulation of smooth muscle tone. Three major mechanisms are involved:

(1)Influx of extracellular calcium through voltageregulated channels;
(2)Activation of membrane-bound receptors which allow extracellular calcium to enter through receptor-operated channels;
(3)Activation of signal pathways which allow intracellular release of calcium from the sarcoplasmic reticulum.

{embed="sex/menu-ed"}
Relaxation of cavernosal smooth muscle may be thought of as 'resetting' the contractile machinery. This is mainly accomplished by lowering intracellular calcium. There are a number of mechanisms by which this may be achieved but, in general, all pathways depend on either the accumulation of cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP), or the activation of potassium channels with consequent hyperpolarization of the cellular membrane (Figure 16).

Nitric oxide, produced from its precursor L-arginine by nitric oxide synthase (NOS), appears to exert two effects within the corpora (Figure 17):

(1)Activation of potassium-channel ATPase, resulting in hyperpolarization of the smooth muscle cell membrane. This hyperpolarization prevents the opening of voltage-dependent calcium channels, thereby reducing intracellular calcium;
(2)Activation of guanylate cyclase which catalyzes the conversion of guanosine triphosphate (GTP) to cGMP. This triggers relaxation by lowering intracellular calcium.

Other muscle relaxants act via cAMP-dependent mechanisms and include prostaglandin (PG) E1 and vasoactive intestinal polypeptide (VIP). These substances react with membrane receptors coupled to a G protein which stimulates adenylate cyclase to produce cAMP, thus lowering intracellular calcium. The presence of two distinct and separate pathways to induce intracorporeal vasodilatation is probably a reflection of the importance of the erectile mechanism in the perpetuation of the species.