TITLE

Nature of the acidifying defect after the relief of ureteral obstruction

AUTHOR(S)
Walls, John; Buerkert, John E.; Purkerson, Mabel L.; Klahr, Saulo
PUB. DATE
January 1975
SOURCE
Kidney International;Jan1975, Vol. 7 Issue 1, p304
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
The acidifying capacity of the normal and experimental kidney was studied in rats three hours after release of complete unilateral ureteral obstruction or after unilateral release of bilateral ureteral obstruction. In seven rats following release of unilateral ureteral obstruction, mean plasma bicarbonate concentration was 23.5 mEq/liter, and plasma pH, 7.45. Urine pH from the postreleased kidney was 7.47 and 6.01 from the control side. Net acid excretion averaged 0.97 ± 0.14 μEq/min in the control and -0.17 ± 0.05 μEq/min in the experimental kidney. Fractional excretion of bicarbonate averaged 0.02% in the control and 3.17% in the experimental kidney. In eight animals with unilateral release of bilateral ureteral obstruction, mean plasma bicarbonate was 16.9 mEq/liter and plasma pH was 7.35. Mean urine pH in the postreleased kidney was 6.11, net acid excretion averaged 2.01 ± 0.69 μEq/min and fractional bicarbonate excretion averaged 0.84%. A third group of animals received ammonium chloride prior to release of unilateral ureteral obstruction. In these animals mean plasma bicarbonate concentration was 16.9 mEq/liter, and plasma pH, 7.32. Urine pH was 5.70 in the control and 5.79 in the experimental kidney. Bicarbonate titration studies in four animals after release of unilateral ureteral obstruction failed to demonstrate a Tm for bicarbonate in either the experimental or control kidney. There was no evidence for an increased splay in the bicarbonate titration curves. Micropuncture experiments failed to demonstrate decreased bicarbonate reabsorption after release of unilateral ureteral ligation in surface nephrons. Urinary PCO2 values remained low after bicarbonate loading in the experimental kidney of rats subjected to release of unilateral ureteral ligation. It is suggested that the acidifying defect may be due to decreased H+ secretion in the distal and collecting duct of surface nephrons or to marked alteration in the reabsorption of bicarbonate in juxtamedullary nephrons.
ACCESSION #
17965893

 

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