Effect of HCO(3)(-) on TPA- and IBMX-induced anion conductances in Necturus gallbladder epithelial cells |
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Authors: | Lyall P Armstrong W M Lyall V |
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Affiliation: | Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis, Indiana 46202-5102, USA. |
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Abstract: | Effects of HCO3 on protein kinase C (PKC)-and protein kinase A (PKA)-induced anion conductances were investigatedin Necturus gallbladder epithelial cells. InHCO3-free media, activation of PKC via12-O-tetradecanoylphorbol 13-acetate (TPA) depolarizedapical membrane potential (Va) and decreased fractional apical voltage ratio (FR). These effects wereblocked by mucosal 5-nitro-2-(3-phenylpropylamino) benzoic acid(NPPB), a Cl channel blocker. In HCO3media, TPA induced significantly greater changes inVa and FR. These effects wereblocked only when NPPB was present in both mucosal and basolateralcompartments. The data suggest that TPA activates NPPB-sensitive apicalCl conductance (gCla) in theabsence of HCO3; in its presence, TPA stimulated bothNPPB-sensitive gCla and basolateralCl conductance (gClb).Activation of PKA via 3-isobutyl-1-methylxanthine (IBMX) also decreased Va and FR; however, thesechanges were not affected by external HCO3. Weconclude that HCO3 modulates the effects of PKC ongClb. In HCO3 medium, TPAand IBMX also induced an initial transient hyperpolarization andincrease in intracellular pH. Because these changes were independent ofmucosal Na+ and Cl, it is suggested that TPAand IBMX induce a transient increase in apical HCO3 conductance. |
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