superior vesical artery.
external iliac artery.
corporal pressure increase (to several hundred millimeters of mercury).
subtunical venous compression reducing venous outflow.
relaxation of the ischiocavernosus muscles.
dilation of the arterioles and arteries.
nitric oxide (NO).
Low cytosolic calcium favors smooth muscle relaxation.
NO released by endothelial nitric oxide synthase (eNOS) contained in the terminals of the cavernous nerve initiates the erection process, whereas nitric oxide released from neuronal nitric oxide synthase (nNOS) in the endothelium helps maintain erection.
NO stimulates the production of cyclic guanosine monophosphate (cGMP).
The smooth muscle regains its tone when cGMP is degraded by phosphodiesterase.
Cyclic GMP activates protein kinase G, which in turn opens the potassium channels and closes the calcium channels.
It increases bone density and lean body mass.
It increases the frequency of sexual acts.
It increases the frequency of nocturnal erection.
It enhances sexual interest.
It increases visually stimulated erections.
NO is the principal neurotransmitter mediating penile erection.
Oxytocin is a potent inducer of erection when injected into the central nervous system.
GABAB receptors are pro-erectile.
Cannabinoid CB1 receptor activation inhibits sexual function.
Central norepinephrine transmission has a positive effect on sexual function.
MLCP inhibition may lead to enhanced smooth muscle contraction.
Myosin light chain phosphatase (MLCP) is a holoenzyme consisting of a type 1 phosphatase (PP1c), a myosin-targeting subunit (MYPT1), and a 20-kDa subunit of unknown function.
Phosphorylation of the regulatory subunit of MLCP by Rho kinase inhibits phosphatase activity and enhances the contractile response.
Latch state refers to a period of smooth muscle relaxation after prolonged contraction.
One of the mechanisms of increased intracellular Ca2 + is by permitting entry of extracellular Ca2 + through receptor-operated channels without a change in membrane potential.
Upregulation of nNOS expression has been found in the corpus cavernosum of aging and diabetic rats.
NOS exists as three isoforms in mammals: nNOS, inducible nitric oxide synthase (iNOS), and eNOS.
Gene transfer of iNOS has enhanced intracavernous pressure.
Synthesis of NO is catalyzed by NOS, which converts l-arginine and oxygen to l-citrulline and NO.
Gene transfer of nNOS or eNOS to the penis has been shown to augment erectile responses in aging rats.
The erectogenic effects of PGE1 as a pharmaceutic agent have been extensively documented.
Protein kinase G-I (PKGI) may induce relaxation via activation of the plasma membrane Ca2 +-ATPase pump, inhibition of IP3 generation, inhibition of Rho-kinase, stimulation of MLCP, and phosphorylation of heat shock proteins.
Reduced penile adenosine levels are associated with priapism.
C-type natriuretic peptide (CNP) is the most potent natriuretic peptide and it relaxes the isolated cavernous smooth muscle by binding to NPR-B.
Calcitonin gene-related peptide is a potent vasodilator released from perivascular nerve fibers.
10% to 19% of cases of ED are neurogenic.
There is a decrease in penile tactile sensitivity with increasing age.
Psychogenic ED is the most common form of ED.
In diabetics, impairment of neurogenic and endothelium-dependent relaxation results in inadequate NO release.
In cases of pelvic fracture, ED can be a result of cavernous nerve injury or vascular insufficiency or both.
Lesions in the pudendal arteries are less common in men with ED than in the general population of similar age.
Common risk factors associated with arterial insufficiency include hypertension, hyperlipidemia, cigarette smoking, diabetes mellitus, blunt perineal or pelvic trauma, and pelvic irradiation.
Among men with coronary arterial disease, the prevalence of ED increases while the severity of coronary arterial lesions increases.
Atherosclerotic or traumatic arterial occlusive disease can decrease the perfusion pressure and arterial flow to the sinusoidal spaces.
Long-distance cycling is also a risk factor for vasculogenic and neurogenic ED.
Diabetes mellitus and metabolic syndrome may affect multiple organ systems and cause premature aging of both central and peripheral structures and molecules that regulate erectile process.
The aging process can affect the central regulatory mechanism, hormonal and neural function, and penile structure.
Primary ED may be due to psychogenic cause, inexperience, congenital arterial insufficiency or abnormal venous channels.
Primary ED refers to a recently developed ED of unknown etiology.
Aging is the single most important contributing factor to ED.
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