The present study was designed to indirectly localize the tubular sites of
carbonic anhydrase independent
bicarbonate reabsorption in the rat. Papillary
necrosis was induced in rats by
intravenous administration of
bromoethyleneamine hydrobromide (BEA) 6 weeks prior to the study, in order to assess the role of deep nephrons in this process.
Acetazolamide alone,
acetazolamide plus
amiloride, and
acetazolamide,
amiloride plus
furosemide were infused into rats with intact papillae (groups I, III, V) and rats with BEA-induced papillary
necrosis (groups II, IV, VI). Our results show that chronic papillary
necrosis does not alter
carbonic anhydrase independent
bicarbonate reabsorption, since the fractional excretion of
bicarbonate (FEHCO3) was not significantly higher when
acetazolamide was infused into animals with BEA-induced papillary
necrosis as compared to those rats with intact papillae (FEHCO3 group I vs. group II: NS). The addition of
amiloride hydrochloride, a blocker of distal acidification at the administered doses, increased FEHCO3 significantly in both, animals with intact papillae and those with papillary
necrosis, to a similar degree. The addition of
furosemide to
acetazolamide and
amiloride further induced a significant increase in FEHCO3 only in the group of animals with papillary
necrosis (FEHCO3 group V 43.0 +/- 2.9% vs. group VI 52.1 +/- 0.9%; p less than 0.05). It appears from our study that deeper nephrons and papillary structures are not indispensable for
carbonic anhydrase independent
bicarbonate reabsorption in the rat on a chronic basis. The cortical collecting duct appears to have a significant capacity to reabsorb
bicarbonate independent of
carbonic anhydrase which can be blocked by
amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)