血浆、腺体及尿液激肽释放酶在链脲佐菌素诱导糖尿病大鼠肾肥大中的相关性

Relevance of plasma, glandular and urinary kallikrein in renal hypertrophy in streptozotocin-diabetic rats.

作者信息

Sulaiman M I, Al-Fayz S F

出版信息

Acta Diabetol Lat. 1986 Jul-Sep;23(3):253-9. doi: 10.1007/BF02624713.

Abstract

The relevance of plasma, glandular and renal kallikrein as an intrarenal hemodynamic regulator, in renal hypertrophy, in 1-5 weeks streptozotocin diabetic rats has been investigated. The fasting plasma glandular kallikrein level significantly decreased with increasing duration of diabetes (p less than 0.05). Glandular kallikrein correlated negatively with kidney weight (r = 0.76, p = 0.05). The 24 hour urinary kallikrein excretion significantly increased with increasing duration of diabetes (p less than 0.05), but this level was not correlated with glucose level, nor with kidney weight. Aprotinin (a kallikrein inhibitor) injected (10 X 10(3) KIU/kg) twice daily for 2 weeks in diabetic rats, significantly decreased plasma glucose levels by 28%, 24 hour urinary kallikrein by 37% (p less than 0.05) and kidney weight by 6%. These results suggest that plasma, glandular and renal kallikrein did not play an important role in the renal hypertrophy observed in streptozotocin diabetic rats.

摘要

研究了血浆、腺体和肾脏激肽释放酶作为肾内血流动力学调节剂在链脲佐菌素诱导的糖尿病大鼠1 - 5周肾肥大中的作用。空腹血浆腺体激肽释放酶水平随糖尿病病程延长显著降低（p < 0.05）。腺体激肽释放酶与肾脏重量呈负相关（r = 0.76，p = 0.05）。糖尿病大鼠24小时尿激肽释放酶排泄量随病程延长显著增加（p < 0.05），但该水平与血糖水平及肾脏重量均无相关性。在糖尿病大鼠中，每天两次注射抑肽酶（一种激肽释放酶抑制剂，10×10³KIU/kg），持续2周，可使血糖水平显著降低28%，24小时尿激肽释放酶降低37%（p < 0.05），肾脏重量降低6%。这些结果表明，血浆、腺体和肾脏激肽释放酶在链脲佐菌素诱导的糖尿病大鼠肾肥大中未发挥重要作用。