The diagram below on the basic mechanisms of erection and flaccidity of the penis also shows the blood supply and innervation of the penis.
The mechanisms of erection and flaccidity are shown in the upper and lower inserts, respectively. During erection, relaxation of the trabecular smooth muscle and vasodilatation of the arterioles results in a severalfold increase in blood flow, which expands the sinusoidal spaces to lengthen and enlarge the penis. The expansion of the sinusoids compresses the subtunical venular plexus against the tunica albuginea. In addition, stretching of the tunica compresses the emissary veins, thus reducing the outflow of blood to a minimum. In the flaccid state, inflow through the constricted and tortuous helicine arteries is minimal, and there is free outflow via the subtunical venular plexus.
Penile erection is a complex physiologic process that occurs through a coordinated cascade of neurologic, vascular, and humoral events.
In the flaccid penis, a balance exists between blood flow in and out of the erectile bodies.
Mechanics of erection. (A) In the flaccid state, arterial vessels are constricted and venous vessels are noncompressed. (B) On erection, smooth muscle relaxation in the trabeculae and arterial vasculature results in increased blood flow, which rapidly fills and dilates the cavernosal spaces. Venous outflow drops as the expanding cavernosal spaces compress the venous plexus and the larger veins passing through the tunica albuginea.
With sexual arousal through imaginative, visual, auditory, tactile, olfactory, and other erotic stimuli, nitric oxide (NO) is released by nonadrenergic, noncholinergic (NANC) neurons. Originally termed endothelial-derived relaxing factor, NO is known to be the most important physiologically occurring vasoactive molecule in the entire cardiovascular system. This also applies to corpus cavernosum function, where local smooth muscle relaxation, and in turn erection, is mediated predominantly by NO release.
On arousal, parasympathetic activity triggers a series of events starting with the release of nitric oxide and ending with increased levels of the intracellular mediator cyclic guanosine monophosphate (cGMP). Increases in cGMP cause penile vascular and trabecular smooth muscle relaxation. Blood flow into the corpora cavernosa increases dramatically. The rapid filling of the cavernosal spaces compresses venules resulting in decreased venous outflow, a process often referred to as the corporeal veno-occlusive mechanism. The combination of increased inflow and decreased outflow rapidly raises intracavernosal pressure resulting in progressive penile rigidity and full erection.
Non-adrenergic, non-cholinergic nerves and vascular endothelium release nitric oxide in response to sexual arousal, which activates cytoplasmic guanylate cyclase, converting GTP into cGMP. The increased levels of cGMP alter transmembrane calcium ion flux, resulting in cavernosal smooth muscle relaxation, dilatation of cavernosal and helicine arteries and engorgement of lacunar spaces. The expanding lacunar spaces compress the subtunical venous plexus against the tunica albuginea, decreasing cavernosal venous outflow, increasing intracavernosal pressure, with resulting penile rigidity. Cyclic nucleotides, such as cGMP, are hydrolysed by cyclic nucleotide phosphodiesterases.
GTP=guanosine triphosphate; GMP=guanosine monophosphate; cGMP=cyclic guanosine monophosphate.
So the basic mechanism underlying is the relaxation of the penile smooth muscle.
Cyclic AMP (cAMP) and cyclic GMP (cGMP), the intracellular second messengers mediating smooth-muscle relaxation, activate their specific protein kinases, which phosphorylate certain proteins to cause opening of potassium channels, closing of calcium channels, and sequestration of intracellular calcium by the endoplasmic reticulum. The resultant fall in intracellular calcium leads to smooth-muscle relaxation. Sildenafil inhibits the action of phosphodiesterase (PDE) type 5, thus increasing the intracellular concentration of cGMP. Papaverine is a nonspecific phosphodiesterase inhibitor. GTP denotes guanosine triphosphate, and eNOS endothelial nitric oxide synthase.
It is well established that NO and cGMP are the most important transmitters for onset and maintenance of erection. Finally, cGMP is metabolized to GMP via phosphodiesterase, of which four isoforms (types 2, 3, 4, and 5) have been identified in human penile tissue. Phosphodiesterase type 5 (PDE 5) is the predominant isoform in human corporal smooth muscle. We shall refer to this again when we discuss the action of sildenafil citrate.
Detumescence.After ejaculation or cessation of erotic stimuli, sympathetic tonic discharge resumes, resulting in contraction of the smooth muscles around sinusoids and arterioles. Arterial flow is diminished to flaccid levels, much of the blood from the sinusoidal spaces is expelled, and the venous channels reopen.
During the return to the flaccid state, cyclic GMP is hydrolyzed to GMP by phosphodiesterase type 5. Other phosphodiesterases are also found in the corpus cavernosum, but they do not appear to have an important role in erection.
Norepinephrine from sympathetic nerve endings, and endothelins and prostaglandin F2 from the endothelium, activate receptors on smooth-muscle cells to initiate the cascade of reactions that results in elevation of intracellular calcium concentrations and smooth-muscle contraction. Protein kinase C is a regulatory component of the calcium-independent, sustained phase of agonist-induced contractile responses.
The key to the entire system is smooth muscle. The percent of smooth muscle dictates the ability to achieve and maintain erections. Roughly 45 percent of the cavernosal body is made up of smooth muscle.The common mechanism of these agents may be via regulation of smooth muscle calcium.
Penile erection or flaccidity is determined by the state of relaxation or contraction of trabecular and arteriolar smooth muscle, which is influenced, in turn, by several factors, including:
Trabecular muscle tone is controlled and penile blood vessel smooth muscle tone may be influenced by three neuroeffector systems.
Local Penile Smooth Muscle Physiologic Mechanisms
In the flaccid state, the smooth muscle cells of the penile arteries and the corpora cavernosa are in a state of tone (contraction). Relaxation of the smooth muscle (arterial and cavernosal) causes increased inflow of blood into the lacunar spaces of the corpora cavernosa. The arterial pressure expands the relaxed trabecular walls, thus expanding the tunica albuginea with subsequent elongation and compression of the draining venules.
This mechanism of veno-occlusion restricts the outflow of blood through these channels. After ejaculation or cessation of the erotic stimuli, the smooth muscle surrounding the arteries and the lacunar spaces contracts. The inflow of blood is reduced and the venous drainage of the corporeal spaces is opened, returning the penis to the flaccid state. Erection of the penis is thus a haemodynamic event under the control of the autonomic nervous system. Coordination of the neuronal activity from psychogenic stimuli occurs in the hypothalamus while reflexogenic erection involves a polysynaptic coordination in the sacral parasympathetic centres.
The mechanisms of erection and detumescence are much more complex than that described above with many other factors and secondary messengers playing a role. But the description above gives the more important an salient points.
Schematic Diagram Of Penile Erection