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A double-membrane model for urinary bicarbonate secretion.

D L Stetson, R Beauwens, J Palmisano

    The American Journal of Physiology
    |October 1, 1985
    PubMed
    Summary
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    This study clarifies bicarbonate (HCO3-) secretion in turtle bladders. Findings reveal a Cl-HCO3 exchanger at the luminal membrane and a 9-AA-sensitive conductance activated by IBMX and cAMP.

    Area of Science:

    • Physiology
    • Cell Biology
    • Renal Physiology

    Background:

    • Understanding ion transport mechanisms is crucial for physiological regulation.
    • Bicarbonate secretion plays a key role in maintaining acid-base balance.
    • The specific pathways for HCO3- transport in turtle bladder are not fully elucidated.

    Purpose of the Study:

    • To define the transport pathway for bicarbonate secretion (JHCO3) across the apical and basolateral membranes of turtle bladder.
    • To investigate the roles of cAMP, IBMX, 9-AA, and DIDS in regulating JHCO3.
    • To elucidate the cellular mechanisms underlying HCO3- transport.

    Main Methods:

    • Measurement of total JHCO3 using pH stat titration.
    • Assessment of short-circuit current (ISC) to evaluate electrogenic components.

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  • Pharmacological inhibition using cAMP, IBMX, 9-AA, DIDS, and acetazolamide.

    • Main Results:

    • cAMP and IBMX increased JHCO3 and induced ISC, with reduced net Cl- absorption.
    • Mucosal 9-AA inhibited the IBMX-induced electrogenic component of JHCO3.
    • Mucosal DIDS inhibited the electroneutral component, while acetazolamide reduced both.

    Conclusions:

    • Bicarbonate is generated by basolateral Na+-independent active transport and accumulates intracellularly.
    • Cellular HCO3- drives JHCO3 via a luminal Cl-HCO3 exchanger.
    • IBMX and cAMP activate a parallel 9-AA-sensitive anion conductance, suggesting a distinct transport system compared to H+-secreting cells.