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sxe Nevertheless, animal studies have provided some basic foundation sed our understanding of erectile physiology and the role vdieo play in this process. In this review, we discuss knowledge sez from animal studies to provide hwving succinct analysis of the cellular, molecular, and physiologic mechanisms of androgens in erectile physiology, and how such knowledge swx be translated into a new clinical paradigm for the management of patients havint androgen deficiency and erectile dysfunction ED. Our objective is to engage readers in a constructive and stimulating debate regarding the use of testosterone in men, and to promote new, innovative basic and clinical research to further understand the underlying cellular and molecular mechanisms of androgen action in restoring erectile physiology.

Modulation of erectile physiology by androgens: Testosterone regulates nerve structure and function The studies of Meusburger and Keast [ 5 ] and Keast et al [ 6 ] have provided elegant demonstrations on the potential role of androgens in maintaining the structure and function of many pelvic ganglion neurons. They suggest that testosterone is critical for the maturation and maintenance of terminal axon density and neuropeptide expression in the vas deferens. Giuliano et al [ 7 ] suggested that testosterone acting peripherally to the spinal cord enhances the erectile response of the cavernous nerve. Rogers et al [ 8 ] demonstrated that castration altered the dorsal nerve ultrastructure in the rat concomitant with loss of erectile function.

The authors further showed that testosterone treatment of castrated animals restored the nerve fibers and myelin sheath structure, similar to that observed in the sham control group. Baba et al [ 910 ] reported that the integrity of NADPH diaphorase-stained nerve fibers in the rat corpus cavernosum and dorsal nerve is dependent on androgens. Recently, we examined the effects of castration on the structural integrity and function of the cavernosal nerve Traish et al, unpublished observations. We noted that there were marked structural changes in the cavernosal nerve from castrated animals compared with control sham-operated animals or castrated animals treated with androgens Fig.

These adul alterations may be responsible in part for the marked reduction in the intracavernosal pressure attenuated blood flow observed in the experimental animals [ 11 ]. In addition, recent studies have demonstrated that penile erection in rats, elicited by stimulation of the medial preoptic area, is testosterone-dependent [ 12 ]. Thus, testosterone may regulate central mechanisms of penile erection, as well as peripheral neural mechanisms.