Studies in the isolated cortical tubule of the rabbit have shown that tubules removed from acidotic rabbits consistently absorb HCO3 in vitro, whereas tubules removed from alkalotic rabbits consistently secrete HCO3. Bladders removed from alkalotic turtles or toads showed enhanced HCO3 for chloride exchange in vitro. The mechanism responsible for adaptive increase in H+ secretion in metabolic or respiratory acidosis is unknown. Ammonia excretion plays an important role in renal acid excretion. The turtle bladder can be utilized to study several aspects of the adaptation to metabolic or respiratory acidosis and ammonia excretion and production, and thus should provide answers to questions not elucidated by previous studies.
The specific aims of this proposal are: a. To examine the effect of metabolic or respiratory acidosis in vivo on urinary acidification (H+ secretion and HCO3 secretion) by the turtle bladder in vitro. b. To examine the mechanism(s) whereby metabolic or respiratory acidosis increases H+ secretion by the turtle bladder in vitro by assessing intracellular pH, surface morphology, fluorescence microscopy, and coupling between metabolism and active transport. c. To examine the regulation of ammonia production by the turtle bladder under normal conditions and during metabolic and respiratory acidosis. These studies will provide insight into the mechanisms whereby metabolic or respiratory acidosis increase H+ secretion and ammonia production.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases (NIADDK)
Type
Research Project (R01)
Project #
5R01AM036253-02
Application #
3154539
Study Section
General Medicine B Study Section (GMB)
Project Start
1985-01-01
Project End
1987-05-31
Budget Start
1985-06-01
Budget End
1986-05-31
Support Year
2
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Illinois at Chicago
Department
Type
Schools of Medicine
DUNS #
121911077
City
Chicago
State
IL
Country
United States
Zip Code
60612
Arruda, J A; Dytko, G; Talor, Z (1990) Stimulation of H+ secretion by CO2 in turtle bladder: role of intracellular pH, exocytosis, and calcium. Am J Physiol 258:R222-31
Arruda, J A; Talor, Z; Dytko, C (1988) Effect of agents that alter cell calcium and microfilaments on CO2 stimulated H+ secretion in the turtle bladder. Arch Int Pharmacodyn Ther 293:273-83
Wheeler, R P; Arruda, J A (1987) Adaptation to metabolic acidosis by turtle urinary bladder. Am J Physiol 252:F256-66
Talor, Z; Yang, W C; Shuffield, J et al. (1987) Chronic hypercapnia enhances Vmax of Na-H antiporter of renal brush-border membranes. Am J Physiol 253:F394-400
Talor, Z; Lubansky, H J; Arruda, J A (1987) Relationship of K and ammonia transport by the turtle bladder. Miner Electrolyte Metab 13:78-84
Yang, W C; Arruda, J A; Talor, Z (1987) Na+-H+ antiporter in posthypercapnic state. Am J Physiol 253:F833-40
Talor, Z; Arruda, J A (1986) Na-Ca exchange in renal tubular basolateral membranes. Miner Electrolyte Metab 12:239-45
Sallman, A L; Lubansky, H J; Talor, Z et al. (1986) Plasma membrane proton ATPase from human kidney. Eur J Biochem 157:547-51