Effect of Metabolic Acidosis on Tubular Proteinase Activity
作者:
Shaoming Huang,
Markus Teschner,
Roland M. Schaefer,
August Heidland,
期刊:
Nephron
(Karger Available online 1994)
卷期:
Volume 66,
issue 3
页码: 344-347
ISSN:1660-8151
年代: 1994
DOI:10.1159/000187834
出版商: S. Karger AG
关键词: Tubule;Acidosis;NH4CI;Proteinases
数据来源: Karger
摘要:
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 NH4C1 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 MNH4Cl treatment, the experimental animals developed mild proteinuria (9.52 ± 0.99 versus 17.65 ± 1.63 mg/day). The kidney weigth 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/μg 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
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