external iliac artery.
superior vesical artery.
dilation of the arterioles and arteries.
corporal pressure increase (to several hundred millimeters of mercury).
subtunical venous compression reducing venous outflow.
relaxation of the ischiocavernosus muscles.
nitric oxide (NO).
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 stimulates the production of cyclic guanosine monophosphate (cGMP).
The smooth muscle regains its tone when cGMP is degraded by phosphodiesterase.
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.
It increases bone density and lean body mass.
It enhances sexual interest.
It increases the frequency of sexual acts.
It increases the frequency of nocturnal erection.
It increases visually stimulated erections.
Cannabinoid CB1 receptor activation inhibits sexual function.
Central norepinephrine transmission has a positive effect on sexual function.
GABAB receptors are pro-erectile.
Oxytocin is a potent inducer of erection when injected into the central nervous system.
NO is the principal neurotransmitter mediating penile erection.
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.
MLCP inhibition may lead to enhanced smooth muscle contraction.
Latch state refers to a period of smooth muscle relaxation after prolonged 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.
Gene transfer of nNOS or eNOS to the penis has been shown to augment erectile responses in aging rats.
NOS exists as three isoforms in mammals: nNOS, inducible nitric oxide synthase (iNOS), and eNOS.
Upregulation of nNOS expression has been found in the corpus cavernosum of aging and diabetic rats.
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.
The erectogenic effects of PGE1 as a pharmaceutic agent have been extensively documented.
Calcitonin gene-related peptide is a potent vasodilator released from perivascular nerve fibers.
C-type natriuretic peptide (CNP) is the most potent natriuretic peptide and it relaxes the isolated cavernous smooth muscle by binding to NPR-B.
Reduced penile adenosine levels are associated with priapism.
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.
Psychogenic ED is the most common form of ED.
In cases of pelvic fracture, ED can be a result of cavernous nerve injury or vascular insufficiency or both.
In diabetics, impairment of neurogenic and endothelium-dependent relaxation results in inadequate NO release.
There is a decrease in penile tactile sensitivity with increasing age.
10% to 19% of cases of ED are neurogenic.
Among men with coronary arterial disease, the prevalence of ED increases while the severity of coronary arterial lesions increases.
Common risk factors associated with arterial insufficiency include hypertension, hyperlipidemia, cigarette smoking, diabetes mellitus, blunt perineal or pelvic trauma, and pelvic irradiation.
Long-distance cycling is also a risk factor for vasculogenic and neurogenic ED.
Atherosclerotic or traumatic arterial occlusive disease can decrease the perfusion pressure and arterial flow to the sinusoidal spaces.
Lesions in the pudendal arteries are less common in men with ED than in the general population of similar age.
Primary ED may be due to psychogenic cause, inexperience, congenital arterial insufficiency or abnormal venous channels.
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.
Aging is the single most important contributing factor to ED.
Primary ED refers to a recently developed ED of unknown etiology.
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