Mechanisms of cation permeation across apical cell membrane ofNecturus gallbladder: Effects of luminal pH and divalent cations on K+ and Na+ permeability

Reuss, Luis; Cheung, Laurence Y.; Grady, Timothy P.

doi:10.1007/bf01875426

Cited by 63 publications

(39 citation statements)

References 29 publications

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“…Similar results were obtained when 10 mM Ba 2+ was added to the luminal saline in order to reduce the K + conductance in the apical membrane. At this concentration Ba 2+ blocks K + channels in the apical membrane ofNecturus (Reuss, Cheung & Grady, 1981) and rabbit gallbladder (unpublished results from this laboratory). The lack of additional effect of Ba 2+ is expected since: i) under control conditions the value of the apical membrane PD is near the K + equilibrium PD so that K + leak toward the lumen is small (Gunter-Smith & Schultz, 1982;Cremaschi, Meyer & Rossetti, 1983); ii) when lumihal K + is removed, V,~ hyperpolarizes, but the K + conductance decreases Garcia-Diaz, Nagel & Essig, 1983); iii) the rate of luminal superfusion is very high and facilitates K + removal in the unstirred layer.…”

Section: K + Removal From the Bathing Fluidsmentioning

confidence: 80%

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

et al. 1987

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In the epithelium of rabbit gallbladder, in the nominal absence of bicarbonate, intracellular Cl- activity is about 25 mM, about 4 times higher than intracellular Cl- activity at the electrochemical equilibrium. It is essentially not affected by 10(-4) M acetazolamide and 10(-4) M 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS) even during prolonged exposures: it falls to the equilibrium value by removal of Na+ from the lumen without significant changes of the apical membrane potential difference. Both intracellular Cl- and Na+ activities are decreased by luminal treatment with 25 mM SCN-; the initial rates of change are not significantly different. In addition, the initial rates of change of intracellular Cl- activity are not significantly different upon Na+ or Cl- entry block by the appropriate reduction of the concentration of either ion in the luminal solution. Luminal K+ removal or 10(-5) M bumetanide do not affect intracellular Cl- and Na+ activities or Cl- influx through the apical membrane. It is concluded that in the absence of bicarbonate NaCl entry is entirely due to a Na+-Cl- symport on a single carrier which, at least under the conditions tested, does not cotransport K+.

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Section: K + Removal From the Bathing Fluidsmentioning

confidence: 80%

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

et al. 1987

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“…Participation of K+ channels in the Clsecretory process has been suggested in a number of studies. Barium, an inhibitor for a number of K+ channels (45)(46)(47)(48)(49)(50), has been found to inhibit electrogenic CF-secretion in frog and piglet gastric mucosa (23,24). Increased basolateral membrane permeability has also been observed, and attributed to K+, during CF-secretion in other epithelial cells (51, 52).…”

Section: Discussionmentioning

confidence: 99%

Chloride secretory mechanism induced by prostaglandin E1 in a colonic epithelial cell line.

Weymer¹,

Huott²,

Liu³

et al. 1985

J. Clin. Invest.

137

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Confluent T8 monolayers grown on permeable supports and mounted in a modified Ussing chamber secrete chloride (Cl-) in response to prostaglandin El. The threshold stimulation was observed at 10-' M and a maximal effect at 10' M. Unidirectional flux studies showed an increase in both serosal to mucosal and mucosal to serosal CI-fluxes with 10' M prostaglandin El; the increase in serosal to mucosal Cl-flux exceeded the increase in mucosal to serosal flux, resulting in net Cl-secretion.Na' transport was not affected in either direction and the changes in net Cla flux correlated well with the changes in short circuit current. To identify the electrolyte transport pathways involved in the Cla secretory process, the effect of prostaglandin El on ion fluxes was tested in the presence of putative inhibitors. Bumetanide was used as an inhibitor for the basolaterally localized Na',K+,Ca-cotransport system whose existence and bumetanide sensitivity have been verified in earlier studies (Dharmsathaphorn et al. 1984. J. Clin. Invest. 75:462-471). Barium was used as an inhibitor for the K+ efflux pathway on the basolateral membrane whose existence and barium sensitivity were demonstrated in this study by preloading the monolayers with "Rb+ (as a tracer for K+) and simultaneously measuring MRb+ efflux into both serosal and mucosal reservoirs. Both bumetanide and barium inhibited the net chloride secretion induced by prostaglandin El suggesting the involvement of the Na+,K+,Ca-cotransport and a K+ efflux pathways on the basolateral membrane in the Clsecretory process. The activation of another Cl-transport pathway on the apical membrane by prostaglandin El was suggested by Cl-uptake studies. Our findings indicate that the prostaglandin El-stimulated Cl-secretion, which is associated with an increase in cyclic AMP level, intimately involves (a) a bumetanide-sensitive Na+,K+,Cl-cotransport pathway that serves as a C1-uptake step across the basolateral membrane, (b) the stimulation of a barium-sensitive K+ efflux mechanism on the basolateral membrane that most likely acts to recycle K+, and (c) the activation of a Cl-transport pathway on the apical membrane that serves as a Cl-exit pathway.

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“…Ordinarily, the apical membrane is the dominant resistance to transepithelial current flow, accounting for 60-90% of the transcellular resistance, although apical membrane resistance can be lowered by numerous factors, including membrane depolarization (Garcia-Diaz et al, 1983;Stoddard and Reuss, 1988b), elevation of intracellular Ca 2+ (Bello- Reuss et al, 1981;Garcla-Diaz et al, 1983) or cAMP levels (Petersen and Reuss, 1983), and extracellular alkalinization . The apical membrane K + conductance in guinea pig gallbladder is also Ca ~+ and voltage sensitive (Gunter-Smith, 1988).…”

Section: Maxi K + Channels In Gallbladder Epitheliummentioning

confidence: 99%

Maxi K+ channels and their relationship to the apical membrane conductance in Necturus gallbladder epithelium.

Segal

Reuss

1990

The Journal of General Physiology

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Using the patch-clamp technique, we have identified large-conductance (maxi) K § channels in the apical membrane of Neaurus gallbladder epithelium, and in dissociated gallbladder epithelial cells. These channels are more than tenfold selective for K § over Na § and exhibit unitary conductance of ~200 pS in symmetric 100 mM KC1. They are activated by elevation of internal Ca 2+ levels and membrane depolarization. The properties of these channels could account for the previously observed voltage and Ca ~+ sensitivities of the macroscopic apical membrane conductance (Ga). Ga was determined as a function of apical membrane voltage, using intracellular microelectrode techniques. Its value was 180/~S/cm ~ at the control membrane voltage of -68 mV, and increased steeply with membrane depolarization, reaching 650 #S/cm 2 at -25 mV. We have related maxi K § channel properties and G a quantitatively, relying on the premise that at any apical membrane voltage G a comprises a leakage conductance and a conductance due to maxi K § channels. Comparison between G~ and maxi K § channels reveals that the latter are present at a surface density of 0.09//zm 2, are open ~15% of the time under control conditions, and account for 17% of control G v Depolarizing the apical membrane voltage leads to a steep increase in channel steady-state open probability. When correlated with patch-clamp studies examining the Ca 2 § and voltage dependencies of single maxi K § channels, results from intracellular microelectrode experiments indicate that maxi K § channel activity in situ is higher than predicted from the measured apical membrane voltage and estimated bulk cytosolic Ca ~ § activity. Mechanisms that could account for this finding are proposed.

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Mechanisms of cation permeation across apical cell membrane ofNecturus gallbladder: Effects of luminal pH and divalent cations on K+ and Na+ permeability

Cited by 63 publications

References 29 publications

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

Chloride secretory mechanism induced by prostaglandin E1 in a colonic epithelial cell line.

Maxi K+ channels and their relationship to the apical membrane conductance in Necturus gallbladder epithelium.

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