Enhancement of Renal Compensatory Hypertrophy by Hyperadrenocorticism and its Modulation by Nutritional Factors

Summary

Renal compensatory hypertrophy (RCH) is enhanced by ACTH in the uninephrectomized rat. In the present experiments, the kidney weight and its content in protein, RNA and DNA were determined in 48 adult, female rats; 24 had free access to a NaCl solution (9 g/l) and the others to a glucose solution (50 g/l). In each group 12 rats were sacrificed 2 or 7 d. after uninephrectomy (UN). In each subgroup 6 rats were treated with ACTH (18 μg/100 g B.W./d) from operation until autopsy. RCH has been evaluated by the arithmetical difference between the data determined in the right control kidney excised at UN and those determined in the left solitary kidney. In all the rats, hyperadrenocorticism increased significantly the weight of the solitary kidney and its content in protein and RNA. There was a significant decrease of the DNA content of the solitary kidney in the rats sacrificed 7 d. post-UN, treated with ACTH and drinking the saline solution. DNA was not affected by ACTH in the 7 other groups suggesting that ACTH favours cellular hypertrophy mainly in the rats drinking the saline solution. The renotrophic action of hyperadrenocorticism may be related to an altered handling of Na⁺ and K⁺: there was a positive correlation between the weight gain of the solitary kidney and the urinary excretion of Na⁺ (r = 0.507, p < 0.001) and of K⁺ (r = 0.460, p < 0.001). Hyperinsulinism was present in all the rats given ACTH; it may act as a growth factor. Hyperglycemia played an important role in former experiments, but it was absent in the present studies.

Key-Words:

Renal Compensatory Hypertrophy - ACTH - NaCl Load - Glucose Load - Kidney Protein, RNA, DNA - Hypernatriuria - K Loss - Hyperinsulinism - Hyperglycemia