Castration and Erection

Sc, Müller; Hsieh, Ju‐Ton; Tf, Lue; Ea, Tanagho

doi:10.1159/000473410

Cited by 39 publications

(27 citation statements)

References 6 publications

(6 reference statements)

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“…Nitric oxide (NO) mediates relaxation of the vascular smooth muscle of the resistance arteries of the corpus cavernosum and the trabeculae to facilitate penile erection. A preponderance of evidence supports a role for androgens in regulating the expression and activity of NOS isoforms in the corpus cavernosum in animal models [14][15][16][17][18][19][20][21][22][23][24][25]. In castrated animals, testosterone or 5α-dihydrotestosterone (DHT) administration restored the erectile response and NOS expression in the penis [9][10][11]16,18,19,21,23,24].…”

Section: Testosterone Regulates Nitric Oxide Synthase Expression and mentioning

confidence: 99%

Testosterone and Erectile Function: From Basic Research to a New Clinical Paradigm for Managing Men with Androgen Insufficiency and Erectile Dysfunction

2007

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Objectives-Androgens are essential for the development and growth of the penis, and they regulate erectile physiology by multiple mechanisms. Our goal is to provide a concise overview of the basic research and how this knowledge can be translated into a new clinical paradigm for patient management. In addition, this new paradigm may serve as a basis for stimulating constructive debate regarding the use of testosterone in men, and to promote new, innovative basic and clinical research to further understand the underlying mechanisms of androgen action in restoring erectile physiology. Methods-A literature review was performed utilizing the US National Library of Medicine's PubMed database.Results-On the basis of evidence derived from laboratory animal studies and clinical data, we postulate that androgen insufficiency disrupts cellular-signaling pathways and produces pathologic alterations in penile tissues, leading to erectile dysfunction. In this review, we discuss androgendependent cellular, molecular, and physiologic mechanisms modulating erectile function in the animal model, and the implication of this knowledge in testosterone use in the clinical setting to treat erectile dysfunction. The new clinical paradigm incorporates many of the consensed points of view discussed in traditional consensed algorithms exclusively designed for men with androgen insufficiency. There are, however, novel and innovative differences with this new clinical paradigm. This paradigm represents a fresh effort to provide mandatory and optional management strategies for men with both androgen insufficiency and erectile dysfunction. Conclusions-The new clinical paradigm is evidence-based and represents one of the first attempts to address a logical management plan for men with concomitant hormonal and sexual health concerns.

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Section: Testosterone Regulates Nitric Oxide Synthase Expression and mentioning

confidence: 99%

Testosterone and Erectile Function: From Basic Research to a New Clinical Paradigm for Managing Men with Androgen Insufficiency and Erectile Dysfunction

2007

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“…30 In dogs, castration leads to a decline in the ratio of intracavernosal pressure to peak systolic pressure and there is also evidence of higher outflow rates in the castrate animals. 31 A decline in the magnitude of the induced intracavernosal pressure rise during erection is observed but the investigators attributed the lower intracavernosal pressure to be accompanying reduction in mean arterial pressure. 31,32 In rabbits, with strips of cavernosal tissue precontracted with a-adrenergic agonists, electrical field stimulation caused a greater degree of relaxation in strips from castrate than from intact animals.…”

Section: Role Of Ischemic Factorsmentioning

confidence: 99%

“…31 A decline in the magnitude of the induced intracavernosal pressure rise during erection is observed but the investigators attributed the lower intracavernosal pressure to be accompanying reduction in mean arterial pressure. 31,32 In rabbits, with strips of cavernosal tissue precontracted with a-adrenergic agonists, electrical field stimulation caused a greater degree of relaxation in strips from castrate than from intact animals. 33 The contraction in response to norepinephrine may also be hormonally dependent, with strips from intact rabbits showing a greater degree of contraction than tissues from castrates in response to the same concentration of the agonist.…”

Section: Role Of Ischemic Factorsmentioning

confidence: 99%

Smooth muscle pathology and erectile dysfunction

Wespes

2002

Int J Impot Res

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Penile erection is a vascular phenomenon that results from smooth muscle relaxation, arterial dilation and venous restriction. The atherosclerosis of the penis that occurs with aging causes a decrease in penile oxygen tension. A reduction of smooth muscle cells has been demonstrated in relation with this change in oxygen tension. Changes in the ratio of penile collagen have also been observed and could explain the decrease in penile elasticity and compliance. Chronic ischemia is, therefore, associated with fibrosis but also with nitric oxide (NO)-cyclic guanosine monophosphate. The sensitivity of the a-adrenoceptors on the smooth muscle cells increases with aging. All those modifications can explain the prevalence of erectile dysfunction with aging. Low oxygen tension in prostanoid production may also play a role in the mechanism of ischemia-induced cavernosal fibrosis; however, intracavernous injections of prostaglandin E 1 do not seem to modify the intracavernous structures by reducing muscular atrophy. The effects of androgen on libido and sexual behavior are well established, but their role in the human erectile mechanism remains unclear. Several studies performed on animals have demonstrated impacts directly on both the physiological function and the trabecular structure of the corpora cavernosa in rats, dogs and rabbits. However, in humans, no study seems to demonstrate a role of testosterone on muscular atrophy or penile neurologic control. Testosterone treatment alters the human behavior but not penile physiologic processes. Further studies are necessary to explain the real role of testosterone not only on the peripheral mechanism of erection but also on the central control.

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“…For detumescence, the smooth muscle of penile arteries and erectile tissue must contract and this hypothalamus, an important site for the modulation of erectile function. However, the local eÂects of castration contraction is probably mediated mainly by the release of noradrenaline acting on post-junctional alpha adrenocepand the resulting low level of testosterone are still unclear and controversial [6][7][8].…”

mentioning

confidence: 99%

Effects of castration on adrenergic, cholinergic and nonadrenergic, noncholinergic responses of isolated corpus cavernosum from rabbit

Yıldırım

Utkan

et al. 1997

British Journal of Urology

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Objective To investigate the eÂects of castration and Endothelium-dependent relaxation elicited by carbachol increased in the castrated group but the relaxtestosterone on the constricting eÂect of phenylephrine and endothelium-dependent and -independent ation induced by sodium nitroprusside did not change and those elicited by adenosine were strongly relaxing eÂects of diÂerent agonists in the corpus cavernosum of male rabbits. depressed when compared with controls. There were no significant changes in the pD 2 values of agonistMaterials and methods Twenty rabbits were castrated and 10 received testosterone replacement for 1 month induced relaxation responses in all groups. The relaxation elicited by electrical-field stimulation at lower after castration; 10 further rabbits underwent a sham operation and acted as controls. One month after frequencies increased in strips from castrated rabbits but at higher frequencies were unchanged when comoperation the rabbits were killed and their penises excised. Strips of corpus cavernosum were used for pared with controls. Castration-induced changes in the relaxation response of cavernosal strips were sigisometric tension measurements in organ chambers; concentration-response relationships for phenylephnificantly restored by in vivo testosterone replacement but those induced by phenylephrine were not. rine, carbachol, adenosine and sodium nitroprusside were obtained by adding the reagent cumulatively to Conclusion The lack of testosterone has an eÂect on the reactivity of the corpus cavernosum, indicating that the bath. Results The phenylephrine-induced contractions were testosterone has an important role in erectile function by a pre-or post-synaptic action on the corpus markedly lower, with no change in the pD 2 values (i.e. the negative logarithm of the concentration for cavernosum.

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Castration and Erection

Cited by 39 publications

References 6 publications

Testosterone and Erectile Function: From Basic Research to a New Clinical Paradigm for Managing Men with Androgen Insufficiency and Erectile Dysfunction

Testosterone and Erectile Function: From Basic Research to a New Clinical Paradigm for Managing Men with Androgen Insufficiency and Erectile Dysfunction

Smooth muscle pathology and erectile dysfunction

Effects of castration on adrenergic, cholinergic and nonadrenergic, noncholinergic responses of isolated corpus cavernosum from rabbit

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