[Modification of the renotrophic action of adrenal hypercorticism by nutritional factors in uninephrectomized rats].

In the rat renal compensatory hypertrophy (RCH) was enhanced by hyperadrenocorticism induced by the administration of a long acting ACTH at a dose of 18 Y/100 g body weight/d. for 7 d. after uninephrectomy (UN). In the present experiments we compared the differences delta between the weight, the content in protein, RNA and DNA of the left solitary kidney and the same determinations done on the right kidney excised at UN 7 d. earlier. The rats drank freely a isotonic solution of NaCl (G1) or KCl (G2) or glucose (G3, G4). The rats of group G1, G2 and G3 received a standard solid food; the G4 rats ate a K poor diet. About half of the animals were treated with ACTH. RCH occurred in all the rats even when they lost body weight. The gain in weight of the solitary kidney was enhanced in all the rats treated with ACTH but not in the G2 rats loaded with KCl. This renotropic action of hyperadrenocorticism was most prominent in the K depleted G4 rats. The protein/DNA ratio, a marker of cellular hypertrophy, was increased by hyperadrenocorticism in the G1 and D2 rats drinking respectively the NaCl or the KCl solutions. This ratio did not change in the ACTH treated G3 and G4 rats drinking the glucose solution suggesting that, in this experimental condition, cellular hyperplasia and hypertrophy occurred at the same extent. These experiments suggest that, in the uninephrectomized rat, the renotrophic action of ACTH is modulated by nutritional factors. The enhancement of RCH by ACTH may be related to hyperglycemia, hyperinsulinism or altered handling of Na and K by the nephron.