BIOCHEMICAL EVALUATION OF COMPENSATORY RENAL HYPERTROPHY

I. Effect(s) of Renotrophic Factor(s) on Nucleic Acid Metabolism of Rat Kidneys

Abstract

The origin and character of the stimulus that initiates compensatory renal hypertrophy and hyperplasia has not been clearly established. The present study was undertaken to measure serum of uninephrectomized rats for activity of a humoral factor(s) which has been postulated to initiate compensatory renal hypertrophy. Serum taken from rats 24, 48 and 72 hours ofter unilateral nephrectomy, when compared to serum taken from sham operated animals, stimulated adenine-8-¹⁴C incorporation into DNA and RNA of rat kidney (in vivo) and kidney slices (in vitro) but not into those of liver (in vivo) and liver slices (in vitro).
These results suggested that a circulating renal growth factor (s) was produced in response to a decrease in renal mass.
It has been suggested that the renotrophically active principles were identical with growth hormone. Therefore, it was investigated how renotrophin (s) was connected with growth hormone, if there were a nexus. Bovine growth hormone stimulated adenine-8-¹⁴C incorporation into DNA and RNA of rat kidney and liver (in vivo), and kidney and liver slices (in vitro). The findings suggested that effects of growth hormone were not organ-specific.
The critical experiment would be to administer serum from hypophysectomized, unilaterally nephrectomized rats (supposedly containing the renotrophic factor(s) of extrahypophyseal origin) to hypopeysectomized rats. The results were obtained that serum from hypophysectomized unilaterally nephrectomized rats stimulated the incorporation of adenine-8-¹⁴C into DNA and RNA of rat kidney slices from hypophysectomized rats, but not into those of liver slices. Based on these findings, the existence of a renotrophic factor(s) which is of a non-hypophyseal origin is postulated.