title: Cellular distribution of H(+)-ATPase following acute unilateral ureteral obstruction in rats.
abstract: Unilateral ureteral obstruction for 24 h produces an acidification defect in the rat kidney that closely resembles the human disorder. We examined the role of renal vacuolar H(+)-ATPase distribution and content in the generation of the postobstructive abnormality in distal hydrogen ion secretion. Rats were subjected to unilateral ureteral obstruction for 24 h, and the obstructed and contralateral kidneys were removed at 3 h, 5 days, and 10 days after release of the obstruction. The postobstructed and contralateral kidneys and kidneys from sham-operated rats were analyzed for intercalated cell number and subtype and for the cellular distribution of ATPase staining by means of a monoclonal antibody specific for the 31-kDa subunit of the vacuolar H(+)-ATPase. No change in the number or distribution of subtypes was detected in the cortex nor in the outer or inner stripe of the outer medulla. Immunoreactive H(+)-ATPase increased in both the cortex and medulla at 3 h after obstruction, and thereafter it declined to control values. The major morphological changes in H(+)-ATPase staining detected were an alteration in the intracellular distribution of the enzyme, which we refer to as discontinuity of (or "gaps" in) apical staining, and a decrease in the percent of intercalated cells showing a rim (or plasma membrane) staining pattern in the inner medulla. The changes observed may be a morphological representation of the physiological abnormalities underlying the postobstructive acidification defect.
authors.affiliation: Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: H
authors.initials: H
authors.lastname: Purcell
authors.forename: B
authors.initials: B
authors.lastname: Bastani
authors.forename: K P
authors.initials: KP
authors.lastname: Harris
authors.forename: P
authors.initials: P
authors.lastname: Hemken
authors.forename: S
authors.initials: S
authors.lastname: Klahr
authors.forename: S
authors.initials: S
authors.lastname: Gluck
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006863:Hydrogen-Ion Concentration; D007668:Kidney / Q000201:enzymology*; D007672:Kidney Cortex / Q000201:enzymology / Q000473:pathology; D007679:Kidney Medulla / Q000201:enzymology / Q000473:pathology; D006180:Proton-Translocating ATPases / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D014517:Ureteral Obstruction / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D014617:Vacuoles / Q000201:enzymology*
chemical_list: D006180:Proton-Translocating ATPases