TITLE

On the mechanism of diminished urinary carbon dioxide tension caused by amiloride

AUTHOR(S)
Hulter, Henry N.; Ilnicki, Leon P.; Licht, J. Hamilton; Sebastian, Anthony
PUB. DATE
January 1982
SOURCE
Kidney International;Jan1982, Vol. 21 Issue 1, p8
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
On the mechanism of diminished urinary carbon dioxide tension caused by amiloride. We investigated under both in vivo and in vitro conditions the mechanism whereby amiloride administration, a model of distal renal tubular acidosis in dogs, decreases the urine-to-blood PCO2 gradient (U-B PCO2.) in alkaline urine. The results demonstrate that U-B PCO2 is reduced in amiloride-induced dogs as previously reported m rats. The reduction in U-B PCO2 could not be attributed to amiloride-induced reductions in urinary HCO3-, concentration since the reduction in U-B PCO2 was observed over the same range of urinary HCO3- concentrations (150 to 250 mEq per liter) as that achieved prior to amiloride administration. U-B PCO2 correlated positively and linearly with urinary HCO3- concentration both prior to (P < 0.001) and during amiloride infusion (P < 0.001). Amiloride administration significantly decreased the slope (∂[U-B PCO2]/<[HCO3-]u) of the regression line (P ∂ 0.005). The possibility that amiloride might lower urine PCO2 by catalyzing intraluminal dehydration of H2CO3 was excluded by demonstrating that amiloride does not possess carbonic anhydrase activity. The additional possibility that amiloride might facilitate dissipation of carbon dioxide gradients through diffusion (as reported for carbonic anhydrase) was excluded by in vitro studies of the effect of amiloride on carbon dioxide diffusion. These findings suggest that the U-B P PCO2 lowering effect of amiloride is not caused by alterations in urinary [HCO3- ], CO2 diffusibility, or alterations in the dehydration rate of H2CO3 thereby providing strong support for the interpretation that reductions in U-B PCO2; during amiloride administration represent an impairment in distal nephron hydrogen ion secretion.
ACCESSION #
17666449

 

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