ABSTRACT
OBJECTIVE: Transforming growth factor-ß (TGF-ß) implicated in the pathogenesis of diabetic nephropathy. Hence, developing agents that antagonize fibrogenic signals is a critical issue facing researchers. MATERIAL AND METHODS: Fifty rats were allocated to five groups: 1=control rats, 2=diabetic hypertensive rats 3=diabetic hypertensive rats treated with spironolactone, 4=diabetic hypertensive rats treated with moexpril, 5=diabetic hypertensive rats treated with both spironolactone and moexpril. Measurement of TGF-ß, aldosterone, creatinine and ACE. Degree of fibrosis was calculated. RESULTS: Serum creatinine, mean arterial blood pressure (MAP), aldosterone, ACE, TGF-ß and renal fibrosis increased significantly in untreated diabetic hypertensive rats compared with control rats. Administration of spironolactone, moexpril, or both decreased these changes. CONCLUSIONS: Addition of the spironolactone to moexpril was more effective in reducing fibrosis and improvement of renal function than monotherapy with either drug, possibly due to a dual inhibitory effect on the RAS, and thus suppression of TGF-ß.
