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 Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK036253-03
Application #
3234557
Study Section
General Medicine B Study Section (GMB)
Project Start
1985-01-01
Project End
1987-06-30
Budget Start
1986-06-01
Budget End
1987-06-30
Support Year
3
Fiscal Year
1986
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
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Kear, F; Ruiz, O S; Arruda, J A (1993) Modulation of renal basolateral Na-phosphate cotransporter by protein kinase A and Ca-dependent protein kinases. Miner Electrolyte Metab 19:373-6
Arruda, J A; Wang, L J; Pahlavan, P et al. (1993) Glucocorticoids and the renal Na-H antiporter: role in respiratory acidosis. Regul Pept 48:329-36
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Pahlavan, P; Wang, L J; Sack, E et al. (1993) Role of protein kinase C in the adaptive increase in Na-H antiporter in respiratory acidosis. J Am Soc Nephrol 4:1079-86
Pahlavan, P; Mejicano, G; Ruiz, O S et al. (1992) Anion channel in basolateral cortical membranes of the rabbit kidney. Miner Electrolyte Metab 18:386-91
Ruiz, O S; Arruda, J A (1992) ATP-dependent renal H+ translocation: regional localization, kinetic characteristics, and chloride dependence. Proc Soc Exp Biol Med 200:562-70
Ruiz, O S; Arruda, J A (1992) Regulation of the renal Na-HCO3 cotransporter by cAMP and Ca-dependent protein kinases. Am J Physiol 262:F560-5
Kniaz, D; Pahlavan, P; Valaitis, D et al. (1991) High-affinity binding sites for VIP in renal cortical membranes: possible role of VIP in renal transport. Kidney Int 39:266-72
Sack, E M; Arruda, J A (1991) Epidermal growth factor binding to cortical basolateral membranes in compensatory renal hypertrophy. Regul Pept 33:339-48

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