Two etiologically different models of experimental
acute renal failure were induced in rats by administration of either
glycerol or
uranyl nitrate. Both compounds caused a substantial decrease in the glomerular filtration rate (GFR) and the net tubular secretion of
tetraethylammonium bromide (
TEAB) and
para-aminohippuric acid (PAH). The degree of renal impairment induced by
uranyl nitrate and
glycerol appeared to be dose related. Deprivation of
drinking water 24 hr before the administration of
glycerol potentiated the renal damage. In
uranyl nitrate-induced
renal failure, the decline of the net tubular secretion for
TEAB and PAH was not proportional to the decrease in GFR; the secretion process deteriorated faster than the GFR. For example, when 0.5 mg/kg
uranyl nitrate was administered, GFR fell to approximately 65% of normal, whereas the net tubular secretion was decreased to 30% of normal. These results suggest that the tubular transport was preferentially affected by
uranyl nitrate. In contrast, in
glycerol-induced
renal failure, the decline of
TEAB secretion fell in a parallel fashion with the GFR, suggesting that the glomeruli and the proximal tubules were equally damaged by
glycerol. However, in this latter model, the decline of PAH secretion did not parallel the decrease in GFR, contradicting the proposal that
glycerol affects equally the glomeruli and the proximal tubules. This discrepancy may be due to the selective competitive inhibition of PAH secretion by the accumulation of naturally occurring organic
acids.(ABSTRACT TRUNCATED AT 250 WORDS)