A primary active, and singly-operating mechanism driving an electrogenic process of luminal alkalinization and another singly-operating mechanism for luminal acidification have been evoked in bladders from alkalotic and acidotic turtles. Both processes are independent of NA or Cl; and cyclic AMP activates the alkalinization function. It is therefore planned to identify those electrochemical and physiological properties which are unique to each mechanism operating at the transepithelial and transmembranal levels, using intact epithelia and membrane vesicle preparations. On the basis of these characterizations, bladders with one or the other acid-base mechanism provide the wherewithal for obtaining new data and insight into the regulation of luminal alkalinization by cyclic AMP, into other aspects of acid-base regulation in this epithelium and presumably in the mammalian nephron.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases (NIADDK)
Type
Research Project (R01)
Project #
5R01AM016928-11
Application #
3151037
Study Section
General Medicine B Study Section (GMB)
Project Start
1978-07-01
Project End
1987-06-30
Budget Start
1985-07-01
Budget End
1986-06-30
Support Year
11
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Mount Sinai School of Medicine
Department
Type
Schools of Medicine
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10029
Schneider, E S; Durham, J H; Matons, C et al. (1988) Alkali secretion in the turtle bladder: up-regulation by the phospho-inositol cascade and inhibition by diphenylamine carboxylate (DPC). Prog Clin Biol Res 258:81-92
Durham, J H; Matons, C; Brodsky, W A (1987) Vasoactive intestinal peptide stimulates alkali excretion in turtle urinary bladder. Am J Physiol 252:C428-35