Adachi Y, Nakada T
Department of Urology, Yamagata University School of Medicine, Japan.
Arch Androl. 1999 Jul-Aug;43(1):37-45. doi: 10.1080/014850199262715.
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.
肾功能不全是性腺功能损害的原因，但睾丸功能障碍的发病机制仍未明确。本研究探讨内分泌紊乱和血管紧张素II诱导的生理异常在两种不同类型慢性肾衰竭性腺功能障碍发病机制中的可能作用。通过给予大鼠高嘌呤饮食或进行5/6肾切除诱导慢性肾功能不全。检测血尿素氮、肌酐、肾素-血管紧张素-醛固酮（R-A-A）系统、雄烯二酮、17α-羟孕酮（17α-OHP）、睾酮、黄体生成素和卵泡刺激素的循环水平。还测定收缩压、肾血流量和睾丸血流量。在血压正常组中，血清17α-OHP、雄烯二酮水平升高，睾酮水平降低。在高血压组中，R-A-A系统增强，睾丸血流量减少，睾酮水平降低。数据表明，腺嘌呤诱导的肾衰竭中的性腺功能障碍似乎是由17β-羟类固醇氧化还原酶活性受抑制引起的，而5/6肾切除所致尿毒症中的性腺损害可由肾素-血管紧张素-醛固酮系统增强和高血压诱发。
