Renal glutaminase adaptation and ammonia excretion in infant rats.
The purpose of this investigation was to determine the role of enzyme adaptation in the response of ammonia excretion to acidosis in developing rats. The response of renal ammonia excretion was low in infant rats (7-12 days old) following administration of a single dose of acidifying salt (5 mmol NH4CL/kg). However, repeated administration (2 times daily) of the salt increased ammonia excretion two- to threefold within 2 days. This adaptive response was associated with a concomitant rise in renal phosphate-dependent glutaminase (PDG) activity; PDG activity increased from approximately 36% adult level in untreated infants to 79% adult level in infants given NH4Cl for 2 days. Ammonia excretion and PDG activity decreased in parallel following cessation of NH4Cl treatment. Administration of the antibiotic, actinomycin D (100 mug/kg, ip, 2 times daily for 2 days) completely inhibited the response of PDG to repeated NH4Cl administration. In contrast to the situation previously observed in adult rats, actinomycin D treatment prevented the acid-induced rise in renal ammonia excretion. These results suggest that the level of renal PDG plays a more direct role in the adaptation of ammonia excretion to acidosis in infant rats than in adults.
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000139:chemically induced; D000222:Adaptation, Physiological; D000367:Age Factors; D000641:Ammonia / Q000652:urine*; D000643:Ammonium Chloride / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D003609:Dactinomycin / Q000494:pharmacology; D005972:Glutaminase / Q000378:metabolism*; D007668:Kidney / Q000201:enzymology* / Q000254:growth & development; D010710:Phosphates / Q000494:pharmacology; D051381:Rats; D013997:Time Factors
D010710:Phosphates; D000643:Ammonium Chloride; D003609:Dactinomycin; D000641:Ammonia; D005972:Glutaminase