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.
|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|