Effects of gonadal hormones on dimorphic striated muscles such as the bulbocavernosus/levator ani complex related to male penile erection have been widely studied. However, the action of these hormones on pelvic nondimorphic muscles is not known. In the present study, the sensitivity of the male rat pubococcygeus muscle (Pcm) to gonadal hormones was studied measuring the cross-sectional area (CSA) of its fibers. For this, two experiments were done: in the first, the effect of castration, and in the second the effect of gonadal hormone administration was analyzed. We found that castration after 6 weeks significantly reduced the average CSA of the fibers of this muscle and that castration after 2 or 6 weeks reduced the percentage of fibers with higher CSAs, but only castration after 6 weeks increased the percentage of fibers with the lowest CSA. In comparison with castrated animals implanted with an empty Silastic capsule, Silastic implants of testosterone propionate or dihydrotestosterone significantly increased the average CSA of Pcm fibers, and the treatment with testosterone propionate, estradiol benzoate, or dihydrotestosterone decreased the percentage of fibers with low CSAs and increased the percentage with larger CSAs. Our results could be considered for therapy in patients with damage of the Pcm, and suffering urinary incontinence or ejaculatory dysfunctions. Anat Rec, 291:586-592, 2008. 2008 Key words: pubococcygeus muscle; dihydrotestosterone; cross-sectional area; estradiol benzoate; testosterone propionate Effects of gonadal hormones on dimorphic striated muscles related to male reproductive physiology have been studied widely, particularly the bulbocavernosus/ levator ani complex implicated in mechanisms of penile erection. It has been shown that androgens affect muscle weight (Tucek et al

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BackgroundThe role of the endothelial cell (EC) in blood flow regulation within the central nervous system has been little studied. Here, we explored EC participation in morphological changes of the anterior hypothalamic paraventricular nucleus (PVN) microvasculature of female rats at two reproductive stages with different metabolic demand (virginity and lactation). We measured the inner capillary diameter (ICD) of 800 capillaries from either the magnocellular or parvocellular regions. The space occupied by neural (somas, dendrites and axons) and glial, but excluding vascular elements of the neurovascular compartment was also measured in 100-μm2 sample fields of both PVN subdivisions.ResultsThe PVN of both groups of animals showed ICDs that ranged from 3 to 10 microns. The virgin group presented mostly capillaries with small ICD, whereas the lactating females exhibited a significant increment in the percentage of capillaries with larger ICD. The space occupied by the neural and glial elements of the neurovascular compartment did not show changes with lactation.ConclusionsOur findings suggest that during lactation the microvasculature of the PVN of female rats undergoes dynamic, transitory changes in blood flow as represented by an increment in the ICD through a self-cytoplasmic volume modification reflected by EC changes. A model of this process is proposed.

The number of fibers in skeletal muscles changes little through life; however, the cross-sectional area of its fibers is modified as result of denervation and in some muscles by castration. The pubococcygeus muscle (Pcm) participates in micturition and ejaculatory processes and its fibers cross-sectional area is reduced in castrated rats, but denervation effects remained unknown. Here, we used a model in which unilateral denervation of this muscle in gonadally intact and castrated male rats, allowed us to explore the neural and gonadal hormone effects on the cross-sectional area of its fibers. Denervation significantly reduced the mean cross-sectional area values; likewise, the percentage distribution of its fibers. We found that castration had a greater effect than denervation. Castration resulted in a lack of fibers from 2,000 to 3,999 lm 2 , while in denervation it was from 2,500 to 3,999 lm 2 . It was interpreted that the castration effect was due to a lack of the direct gonadal hormone effect on muscle fibers, and to a reduction of the indirect hormonal action in its neuromuscular complex. In denervated Pcm of gonadally intact animals these effects were present; however, in denervated but castrated animals these were absent. Thus, combined surgeries resulted in the lowest mean cross-sectional area values with a restricted fiber distribution from 500 to 1,499 lm 2 . In conclusion, the study in this important muscle showed that cross-sectional area of its fibers depends on neural and direct/indirect gonadal hormone effects.

In this study, we analyzed the effect of ovariectomy and gonadal hormone replacement on the cross-sectional area of pubococcygeus (Pcm) fibers. It was found that in comparison to intact animals, ovariectomized animals [for 2 or 6 weeks] had an increased cross-sectional area average in Pcm fibers. Ovariectomy also reduced the percentage of fibers with smaller cross-sectional area. In ovariectomized animals after 4 weeks of hormone replacement with an empty Silastic capsule or filled with testosterone propionate or dihydrotestosterone, significantly increased the cross-sectional area average and the percentage of fibers with larger size. However, 17b-estradiol but not estradiol benzoate treatment reduced the cross-sectional area average and increased the percentage of Pcm fibers with smaller size. Progesterone did not have an effect on the cross-sectional area of this muscle. We conclude that Pcm fibers of female rats are sensitive to gonadal hormones, and contrary to male castration, ovariectomy promotes an increase in their cross-sectional area. Also, we discuss according to other studies that an external mechanism which lies within the neuromuscular periphery could also participate in the modulatory hormonal effect on mass or muscle fiber size. Furthermore, in this process, estradiol is likely to regulate the fiber cross-sectional area growing produced by androgens. Anat Rec, 294:1242Rec, 294: -1248Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.