Effect of metabolic acidosis on tubular proteinase activity.
Metabolic acidosis is a well-known mediator of compensatory renal hypertrophy; however, the underlying mechanism is still poorly understood. The aim of the present study was to investigate whether metabolic acidosis can influence the proteolytic activity in the proximal tubule. Metabolic acidosis was induced in rats by 0.28 M NH4Cl which was mixed to drinking water. The development of metabolic acidosis was documented by a significant increase in urinary pH. After 11 days of 0.28 M NH4Cl treatment, the experimental animals developed mild proteinuria (9.52 +/- 0.99 versus 17.65 +/- 1.63 mg/day). The kidney weight increased significantly (1,653.56 +/- 27.84 versus 1,753.33 +/- 56.11 mg) and tubular proteinase activity, measured at pH 5.4, was markedly reduced (60.3 +/- 1.2 versus 52.2 +/- 2.4 U/mg protein, or 2,105.5 +/- 92.0 versus 1,631.0 +/- 97.2 mU/micrograms DNA). In summary, these results suggest that compensatory renal hypertrophy induced by metabolic acidosis might at least partly be due to the suppression of tubular proteinase activity.
Huang
S
S
Department of Medicine, University of Würzburg, FRG.
Teschner
M
M
Schaefer
R M
RM
Heidland
A
A
D000141:Acidosis, Renal Tubular / Q000139:chemically induced / Q000201:enzymology* / Q000503:physiopathology; D000643:Ammonium Chloride; D000818:Animals; D004195:Disease Models, Animal; D010450:Endopeptidases / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D006984:Hypertrophy / Q000209:etiology; D007668:Kidney / Q000473:pathology; D007687:Kidney Tubules, Proximal / Q000201:enzymology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D000643:Ammonium Chloride; D010450:Endopeptidases