Compensatory renal growth in the mouse. II. The effect of growth hormone deficiency.

Abstract

Allometry was used to study the effect of growth hormones (GH) deficiency on compensatory renal growth (CRG) in a dwarf mouse strain (Little). Nucleic acid and protein estimations were used to assess changes in cellular hyperplasia and hypertrophy. Nephrectomy was performed at 5, 15, or 35 days of age with removal of the renoprival kidney 15 days later. Controls underwent sham nephrectomies at 35 days of age. The allometric growth of the normal kidney in the homozygote dwarf (lit/lit) between 8 and 50 days of age was closely related to that of the normal heterozygote (lit/+). A regression line for the renoprival kidneys in lit/lit animals was parallel to that of the control right kidney (P less than 0.001). The interval between the regression lines was equivalent to a constant difference of approximately 40% between renoprival and control right kidneys and was similar to that found in the normal heterozygote (43%). Increases in DNA, RNA, and protein in control animals during CRG indicate that cell division and hypertrophy were occurring in similar proportions. In the GH-deficient mouse, the total amount of DNA in renoprival kidneys was 0.451 mg compared with 0.439 mg in controls (NS). This suggests that cell replication was suppressed. The protein:DNA ratio increased from 20.91 to 24.27 (P less than 0.001) and the RNA:DNA ratio increased from 0.732 to 0.912 (P less than 0.001), suggesting that cell size was markedly increased. These findings suggest that reduced amounts of GH may produce a dissociation between hyperplasia an hypertrophy, with CRG occurring predominantly by cellular hypertrophy.