Effect of experimentally induced renal failure on testicular testosterone synthesis in rats.

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.