![Sample our Medicine, Dentistry, Nursing & Allied Health journals, sign in here to start your FREE access for 14 days]({"type":"image" , "src" : "/sda/5944/TOC-Subject-Sample-2021-Medicine-Dentistry-Nursing-Allied-Health.jpg"})
Abstract
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 adenineexcessive diet or in 5/6 nephrectomized animals. Circulating levels of blood urea nitrogen, creatinine, renin-angiotensin-aldosterone (R-A-A) system androstenedione, 17alpha-hydroxy progesterone (17alpha-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 17alpha-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 17beta-hydroxysteroid oxydoreductase activity, and gonadal impairment in 5/6 nephrectomized uremia can be evoked by enhanced renin-angiotensin-aldosterone system and hypertension.