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Introduction: Vascular endothelial growth factor (VEGF) is known to influence testis function. Transforming growth factor alpha (TGF-α) is expressed in the postnatal testis, and has been demonstrated to stimulate testis development. Systemic diseases such as chronic renal failure (CRF) interfere with hypothalamic-pituitary-gonadal axis, which may cause defective steroidogenesis and gonadal functions. The aim of this study was to investigate the expression and localization of VEGF and TGF-α in testicular tissues of experimental CRF model., Material and Methods: Experimental CRF was induced in rats by the resection of more than 85% of renal mass. The expression of VEGF and TGF-α in testicular tissues were assessed by immunohistochemistry on paraffin sections of control, CRF-nondialysed and CRF-dialysed rats., Results: The microscopic evaluation of the testicular structure showed that CRF did not affect testicular histology. Immunohistochemical evaluation showed that VEGF was expressed in the cytoplasm of primary and secondary spermatocyte series as well as the early spermatids. Staining intensity was lower in spermatocytes going through the first meiotic division. TGF-α was expressed in the nuclei of spermatogonia and primary spermatocytes with stronger staining intensity in spermatogonia. The intensity of VEGF staining was similar in control and experimental animals, however, TGF-α expression was lower in the CRF group., Conclusions: The continuous expression of VEGF in spermatocytes and spermatids suggests that the applied model of CRF does not directly disrupt morphology of seminiferous epithelium, thus also spermiogenesis. However, difference between control rats and CRF group in TGF-α immunopositivity, which was localised in spermatogonial mitosis step, may suggest the interference of CRF with early stages of spermatogenesis.

Background: The role of nitric oxide in the pathogenesis of renal injury has begun to be appreciated. We therefore designed this study to demonstrate the relationship between endothelial nitric oxide synthase (eNOS) expression and doxazosin in the kidneys of rats with surgically created partial bladder outlet obstruction (BOO), to further understand the role of doxazosin in the prevention of renal parenchymal damage by partial BOO., Material and Methods: A total of 35 adult female Wistar rats, mean weight 250 g, were randomly allocated to 3 experimental groups: group1, sham-operated (n=10); group 2, partial BOO group (n=14) and group 3, partial BOO group treated with doxazosin (n=11). Partial BOO in rats was surgically induced. Results were assessed by eNOS immunohistochemistry., Results: eNOS staining in kidneys in group 1 (16.45 ± 1.63) was significantly higher than in group 2 (5.09 ± 0.61) (p<0.05). After 15 days of doxazosin treatment in addition to partial BOO (group 3), eNOS staining in the kidney (11.80 ± 1.63) was significantly higher than in group 2 (5.09 ± 0.61) (p<0.05). In samples taken after 15 days of doxazosin treatment in addition to partial BOO, eNOS staining in kidneys (11.80 ± 1.63) was lower than in the sham-operated group (16.45 ± 1.63), but the difference was not significant (p>0.05)., Conclusion: These findings may provide insight into the beneficial and restorative effects of α(1)-adrenoceptor antagonists on eNOS expression in the kidney, when used to treat symptoms of benign prostate hyperplasia and hypertension.