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Alkali secretion in the turtle bladder: up-regulation by the phospho-inositol cascade and inhibition by diphenylamine carboxylate (DPC).

The presently reported studies of factors involved in the regulation of acid-base excretory processes in isolated turtle urinary bladders have yielded the following data. (i) There exists in alkalotic and euhydric turtle bladders (but not in acidotic turtle bladders) a mechanism which drives a primary active electrogenic secretion of alkali; and the electrogenic output of this mechanism is up-regulated by exogenously added PDE inhibitors, such as theophylline or IBMX. (ii) VIP or cAMP up-regulates this alkali secretion in the presence of IBMX. (iii) Carbachol also initiates alkali secretion. But this action, independent of PDE activity, is probably associated with the phospho-inositol reaction cascade. (iv) Finally, low concentrations of mucosal DPC decreases the carbachol supported, but not the cAMP-supported alkali secretion.