Ureteral obstruction decreases ATP dependent H(+)-pump activity of rabbit renal outer medulla.
Ureteral obstruction has been known to cause a renal acidification defect. To determine the underlying mechanisms of this defect, vacuolar-type H(+)-pump activity of the membrane vesicles taken from the rabbit renal outermedulla was measured in 24 hr obstructed and contralateral kidneys. H(+)-pump activity measured by acridine orange quenching method was resistant to oligomycin (10 micrograms/ml), vanadate (0.1 mM), and the absence of ambient K+, and it was highly sensitive to N-ethylmaleimide (0.5 mM) and dicyclohexylcarbodiimide (0.2 mM). H(+)-pump activity was 6.69 +/- 1.40 in the obstructed kidney, which was significantly lower than 10.32 +/- 1.88% AFU/mg.min in the contralateral kidney. In sham-operated rabbits, H(+)-pump activities were not different in both kidneys. Passive H+/OH- permeability measured by the rate of dissipation of the imposed pH gradient was not different in obstructed and contralateral kidneys. These results suggest that ureteral obstruction decreases vacuolar-type H(+)-pump activity of the kidney outermedulla, and this decrease may contribute to the distal acidification defect of obstructed uropathy.
Kanemitsu
H
H
Second Department of Internal Medicine, Tokyo Medical and Dental University.
Sasaki
S
S
Akiba
T
T
Marumo
F
F
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D005033:Ethylmaleimide / Q000494:pharmacology; D005260:Female; D006859:Hydrogen / Q000493:pharmacokinetics*; D007679:Kidney Medulla / Q000187:drug effects / Q000201:enzymology*; D011817:Rabbits; D014517:Ureteral Obstruction / Q000378:metabolism*
D006859:Hydrogen; D000251:Adenosine Triphosphatases; D005033:Ethylmaleimide