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Renal insufficiency is responsible for gonadal impairment, but the pathogenesis of testicular dysfunction remains unresolved. This study examines the possible role of the endocrine disturbance and angiotensin II-induced physiological abnormality for the pathogenesis of gonadal dysfunction of two different types of chronic renal failure. Chronic renal insufficiency was induced in rats given an adenine-excessive diet or in 5/6 nephrectomized animals. Circulating levels of blood urea nitrogen, creatinine, renin-angiotensin-aldosterone (R-A-A) system androstenedione, 17 alpha-hydroxy progesterone (17 alpha-OHP), testosterone, luteinizing hormone, and follicle-stimulating hormone were assayed. Systolic blood pressure, renal blood flow, and testicular blood flow were also determined. High serum levels of 17 alpha-OHP, androstenedione, and low testosterone were noted in the normotensive group. Enhanced R-A-A system decreased testicular blood flow and low testosterone were seen in the hypertensive group. The data provide evidence that gonadal dysfunction in adenine-induced renal failure appears to be caused by the suppression of 17 beta-hydroxysteroid oxydoreductase activity, and gonadal impairment in 5/6 nephrectomized uremia can be evoked by enhanced renin-angiotensin-aldosterone system and hypertension.
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Nakada et al. (1999) studied this question.
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