external iliac artery.
superior vesical artery.
dilation of the arterioles and arteries.
relaxation of the ischiocavernosus muscles.
subtunical venous compression reducing venous outflow.
corporal pressure increase (to several hundred millimeters of mercury).
nitric oxide (NO).
NO stimulates the production of cyclic guanosine monophosphate (cGMP).
Cyclic GMP activates protein kinase G, which in turn opens the potassium channels and closes the calcium channels.
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.
The smooth muscle regains its tone when cGMP is degraded by phosphodiesterase.
It increases the frequency of nocturnal erection.
It increases the frequency of sexual acts.
It increases bone density and lean body mass.
It increases visually stimulated erections.
It enhances sexual interest.
Central norepinephrine transmission has a positive effect on sexual function.
GABAB receptors are pro-erectile.
Cannabinoid CB1 receptor activation inhibits sexual function.
NO is the principal neurotransmitter mediating penile erection.
Oxytocin is a potent inducer of erection when injected into the central nervous system.
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.
MLCP inhibition may lead to enhanced smooth muscle contraction.
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.
Phosphorylation of the regulatory subunit of MLCP by Rho kinase inhibits phosphatase activity and enhances the contractile response.
Upregulation of nNOS expression has been found in the corpus cavernosum of aging and diabetic rats.
Gene transfer of nNOS or eNOS to the penis has been shown to augment erectile responses in aging rats.
Gene transfer of iNOS has enhanced intracavernous pressure.
NOS exists as three isoforms in mammals: nNOS, inducible nitric oxide synthase (iNOS), and eNOS.
Synthesis of NO is catalyzed by NOS, which converts l-arginine and oxygen to l-citrulline and NO.
Calcitonin gene-related peptide is a potent vasodilator released from perivascular nerve fibers.
The erectogenic effects of PGE1 as a pharmaceutic agent have been extensively documented.
C-type natriuretic peptide (CNP) is the most potent natriuretic peptide and it relaxes the isolated cavernous smooth muscle by binding to NPR-B.
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.
In cases of pelvic fracture, ED can be a result of cavernous nerve injury or vascular insufficiency or both.
There is a decrease in penile tactile sensitivity with increasing age.
In diabetics, impairment of neurogenic and endothelium-dependent relaxation results in inadequate NO release.
10% to 19% of cases of ED are neurogenic.
Psychogenic ED is the most common form of ED.
Long-distance cycling is also a risk factor for vasculogenic and neurogenic ED.
Among men with coronary arterial disease, the prevalence of ED increases while the severity of coronary arterial lesions increases.
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.
Atherosclerotic or traumatic arterial occlusive disease can decrease the perfusion pressure and arterial flow to the sinusoidal spaces.
Aging is the single most important contributing factor to ED.
Primary ED may be due to psychogenic cause, inexperience, congenital arterial insufficiency or abnormal venous channels.
The aging process can affect the central regulatory mechanism, hormonal and neural function, and penile structure.
Primary ED refers to a recently developed ED of unknown etiology.
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.
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