Role of testosterone in control of erections in VS .NET

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Role of testosterone in control of erections
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Data from experiments in animals: Studies in rodents suggest that besides its well-known effects on the brain centers of sexual function, especially the hypothalamic preoptic area and arcuate nucleus, T plays a key role in the peripheral modulation of erectile function It is well known that the nitric oxide (NO) pathway is critical for initiation and maintenance of erections In animals, the expression of both the endothelial and neuronal NO synthases (NOS), and therefore the capacity for NO production, is regulated by androgens [43,44] Androgen suppression via castration results in marked decrease in NOS activity and cyclic guanosine monophosphate (cGMP) formation, through both NOS-dependent and -independent mechanisms, as well as in profound structural changes in penile tissue (atrophy con-
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Hormones, Metabolism, Aging, and Men s Health ment of all aspects of sexual function was found in men with low (<7 nmol/L, 2 ng/mL) and low normal T (7 12 nmol/L, 2 346 ng/mL) receiving standard replacement doses of T, with respect to placebo Concerning erectile function, the magnitude of the effect was inversely related to the baseline T concentration and was detectable only in studies with mean baseline T level < 12 nmol/L (346 ng/mL) No statistically signi cant effect on libido (though close to signi cance) or erections was found in studies with mean baseline T level above this The type of T preparation used, the length of follow-up assessment, as well as the presence of ED and other co-morbidities (diabetes mellitus, hypertension, dyslipidemia), all in uenced response to treatment The effect of age was not studied in this metaanalysis Although this data suggests a signi cant effect of T therapy on erectile function in cases of marked or moderate hypogonadism, the effects reported in the literature regarding this treatment have been mostly disappointing when it was used alone in middle-aged patients consulting for ED who are subsequently found to be hypogonadal This situation may be quite different from that of men with organic hypogonadism, diagnosed earlier in life, who constitute the majority of the populations studied in RCTs No controlled trial has been speci cally devoted to such patients, but the compilation of eight observational studies totalling 259 cases (T < 3 ng/mL or 115 nmol/L) leads to the conclusion that only 36% were de nitely improved regarding their erectile function [18,20,54 59] Perhaps TT is a poor index of androgenicity, and only its bioavailable fractions should be taken into account This speculation was not con rmed by the results of T therapy in ED patients with low levels of FT or BT, since the success rate was even poorer in this category, including cases that had low FT or BT and normal TT levels [23,60] Probably the low T level of some ED patients is not the real, or at least the sole cause of their ED The lability of serum T has to be considered, and every low result should be con rmed by a second determination In addition, ED is often multifactorial, and the meta-analysis by Isidori et al found that comorbidities in uence the effect of T therapy [53] Signi cant vascular factors, such as obstruction of the penile arteries or venoocclusive dysfunction
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were found in as many as 42% of ED patients with low T levels [18] More subtle alterations such as endothelial dysfunction, probably exist due to many other medical co-factors, and this may also hamper the effects of T therapy It is even probable that in certain cases low T is more a consequence than the cause of ED In two studies the low serum T increased following successful non-hormonal ED therapies (such as intracavernosal or phosphodiesterase type 5 inhibitor (PDE5i) therapies) [25,26] In such cases the reduction in T secretion was likely caused by reduced sexual activity (that has been shown to stimulate T secretion) [61], and by the stress and depression that often result from ED, through the well-known inhibitory impact of the two latter factors on the hypothalamic gonadotropic centers [62,63] Carosa et al observed a reduction in the bioavailability of LH in ED patients that could result from a spacing out of the LHRH pulses via a psychosomatic mechanism, since it was also reversible with successful non-hormonal ED therapies [64] Possible requirement of a minimum serum T level for a complete effect of PDE5i in ED patients: cGMP, the key intracavernosal signal for the relaxation of the cavernosal smooth muscle and thus erection, is inactivated by the enzyme PDE5, present in the cavernous bodies This limits the effects of NO release on erection By inhibiting PDE5, intracavernosal cGMP accumulation occurs, and that often improves the quality of erection In rodents androgens modulate not only the expression of NOS but also that of PDE5 [65,66], as well as the response to electrostimulation of the corpora cavernosa [67] In animal models, it was demonstrated that normal androgen levels are a prerequisite for proper functioning of PDE5i [67,68] The critical importance of a normal T level for intrapenile mechanisms of erection has not been proved until now in humans, but the expression of PDE5 is T-dependent in humans too [66] In addition in a group of ED patients without any other apparent cause of ED than severe hypogonadism, the PDE5i sildena l failed to improve the blunted erectile response to visual sexual stimulation, as it did in eugonadal psychogenic ED patients This response was subsequently restored following T substitution for six months [50] Lastly in another study sildena l improved sleep-related erections even in hypogonadal
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18 because of the small size of the patient sample and the rather high drop-out rate However the speculation that a certain threshold level of T is required for a complete effect of PDE5i has still to be con rmed in larger studies
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men, but the effect of sildena l and T was greater than the sum of the two compounds alone [69] Several uncontrolled studies recently reported an increased prevalence of low or low normal T levels in ED patients who were non-responders to PDE5i, with a frequent improvement of their response following T substitution [70 72] The speculation that hypogonadism was responsible for the PDE5i failure is supported by two controlled studies Aversa et al studied 20 patients (mean age 55) with arteriogenic ED and both TT and FT in the lower quartile of normal range [52] These had been non-responders to six trials with 100 mg sildena l and were randomized to T or placebo patches combined with sildena l on demand With respect to placebo, T-treatment signi cantly increased the arterial in ow to cavernous bodies (peak systolic velocity measured with CDU following sildena l administration), as well as increased scores of the erectile function, intercourse satisfaction, and overall satisfaction domains of the international index of erectile function (IIEF) The Shabsigh et al study (Fig 182) involved more ED patients (75) with low or low normal TT ( 4 ng/mL) non-responders to sildena l 100 mg [73] They were randomized to T or placebo gels combined with sildena l on demand during this time, for 12 weeks After four weeks the scores of the erectile function, orgasmic function, and overall satisfaction domains of the IIEF, as well as the number of patients reporting that their gel improved their response to sildena l, were signi cantly higher in the T group However the statistical differences between the T and placebo groups waned or disappeared at eight and 12 weeks, probably in part
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