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.
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