Cyclic AMP-induced chloride permeability in the apical membrane of Necturus gallbladder epithelium.

Petersen, Karl‐Uwe; Reuss, Luis

doi:10.1085/jgp.81.5.705

Cited by 123 publications

(102 citation statements)

References 36 publications

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“…In contrast with these observations, Duffey et al (1981), in a study primarily designed to assess the effect of CAMP on the junctional complexes of Necturus gallbladder epithelium, found a moderate depolarization of the cell membranes and a large fall in the ratio of cell membrane resistances (apical:basolateral). We subsequently confirmed these results and showed, from measurements of membrane voltages, membrane conductances, and intracellular Cl-activity, that CAMP activates an apical membrane Clconductance (Petersen and Reuss, 1983).…”

Section: Introductionsupporting

confidence: 73%

“…These results are consistent with the hypothesis that the elevation of intracellular cAMP levels inhibits apical membrane Cl-/HCO3 exchange. It must be noted, however, that the ionic composition of the intracellular compartment is different in control and in theophyllinetreated preparations (Petersen and Reuss, 1983;Reuss and Petersen, 1985). Therefore, it is possible that the reduction in HCO-3 efflux in these experiments is due to a reduction of the net driving force for anion exchange.…”

Section: Extracellular Ph Measurementsmentioning

confidence: 86%

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Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Reuss

1987

The Journal of General Physiology

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Intracellular microelectrode techniques were employed to study the effect of cyclic AMP on apical membrane Ci-/HCOi exchange and electrodiffusive HCOi transport in Necturus gallbladder epithelium, lntracellular cAMP levels were raised by addition of either the phosphodiesterase inhibitor theophyiline (3 x 10 -s M) or the adenylate cyclase activator forskolin (10 -5 M) to the serosal bathing solution. Measurements of pH in a poorly buffered control mucosal solution upon stopping superfusion show acidification, owing to secretion of both H + and HCOL When the same experiment is performed after addition of amiloride or removal of Na + from the mucosal bathing medium, alkalinization is observed since H + transport is either inhibited or reversed, whereas HCOi secretion persists. The changes in pH in both amiloride or Na-free medium were significantly decreased in theophylline-treated tissues. Theophylline had no effect on the initial rates of fall of intracellular CIactivity (aCl 0 upon reducing mucosal solution [CI-] to either 10 or 0 mM, although membrane voltage and resistance measurements were consistent with stimulation of apical membrane electrodiffusive CI-permeability. Estimates of the conductive flux, obtained by either reducing simultaneously mucosal [CI-] and [HCOg] or lowering [C1-] alone in the presence of a blocker of anion exchange (diphenylamine-2-carboxylate), indicate that elevation of intracellular cAMP inhibited the anion exchanger by ~50%. Measurements of net CI-uptake upon increasing mucosal C1-from nominally zero to levels ranging from 2.5 to 100 mM suggest that the mechanism of inhibition is a decrease in Vmax. Consistent with these results, the rate of intracellular alkalinization upon reducing external C1-was also inhibited significantly by theophylline. Reducing mucosal solution [HCO~] from 10 to 1 mM under control conditions caused intracellular acidification and an increase in aCll. Theophylline inhibited both changes, by 62 and 32%, respectively. These data indicate that elevation of intracellular cAMP inhibits apical membrane anion (CI-/HCOg) exchange. Studies of the effects of rapid changes in mucosal [HCOg] on membrane voltages and the apparent ratio of membrane resistances, both in the presence and in Address reprint requests to Dr.

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Section: Introductionsupporting

confidence: 73%

Section: Extracellular Ph Measurementsmentioning

confidence: 86%

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Reuss

1987

The Journal of General Physiology

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“…A cyclic AMP induced increase in Cl conductance in the apical membrane of Necturus gallbadder epithelium has been observed using electrophysiological methods (Petersen & Reuss, 1983). This view is corroborated by the following results: (a) the rate of exit of "Br from theophylline-treated tissue is enhanced (Table 4); (b) the rate of exit of mannitol across the mucosal surface seen in the presence of theophylline is increased (Table 5).…”

Section: Discussionmentioning

confidence: 52%

Effects of theophylline, choleragen and loperamide on rabbit ileal fluid and electrolyte transport in vitro

Ahsan

Ilundain

Naftalin

et al. 1987

British J Pharmacology

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1The effects of theophylline and cholera toxin on water and anion movements across rabbit ileum in vitro and the reversal of these effects by the opiate action of loperamide have been investigated. Water movement across the mucosal and serosal surfaces of the tissue was measured continuously by a high resolution method. 2 Theophylline caused an increase in short circuit current and reversed the direction of net Cl1 movement, due mainly to a decrease in mucosal-serosal flux. It also caused a rapid, but transient, reversal in the direction of fluid movement across the mucosal surface. Fluid outflow across the serosal surface was decreased but not reversed. Cholera toxin caused a slow inhibition of water movement across both mucosal and serosal surfaces. 3 Theophylline increased the exit rate of"Br across the mucosal surface and decreased the exit rate of "Br across the serosal surface. Theophylline increased the exit rate of 3H-labelled mannitol across the mucosal surface. 4 Loperamide reversed the effects of theophylline and cholera toxin on water flow across the mucosal and serosal surfaces and on net transepithelial Cl-flux; it also increased the rate of "Br exit across the serosal surface of theophylline-treated tissue. These effects of loperamide could be reversed by naloxone.5 The hydraulic conductivity, Lp of the serosal surface was measured directly by determining the osmotic flow generated by low concentrations of polyethylene glycol (mol. wt. 20000 and 90000).Theophylline reduced the Lp by 57%. Loperamide added to theophylline-treated tissues increased the Lp by 340%. This effect was reversed by naloxone.6 These results indicate that modulation of intestinal smooth muscle tone affects transepithelial ion and water flows in vitro. The increase in tone induced by secretagogues increases ion and water reflux via wide shunt channels in the mucosa and thereby reduces net absorption. The increased net fluid and electrolyte absorption induced by loperamide results from the opiate-dependent inhibition of acetylcholine release from intrinsic ganglia which reduces smooth muscle tone and thereby enhances the fluid and electrolyte conductance of the submucosal layers.

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“…In epithelial cells, [Cl Ϫ ] i is determined by the steady-state relationship between Cl Ϫ transporters in apical and basolateral membranes (25) (47), spiny dogfish rectal gland tubules (22), canine trachea (53), and human colonic epithelium (7,39), but [Cl Ϫ ] i increases with stimulation in human colonic epithelial cells (37).…”

mentioning

confidence: 99%

Inhibition of ENaC by intracellular Cl⁻in an MDCK clone with high ENaC expression

Xie

Schafer

2004

American Journal of Physiology-Renal Physiology

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We examined the effects of intracellular Cl− concentration ([Cl−]i) on the epithelial Na channel (ENaC) in a line of Madin-Darby canine kidney (MDCK) cells (FL-MDCK) with a high rate of Na+ transport produced by stable retroviral transfection with rENaC subunits (Morris RG and Schafer JA. J Gen Physiol 120: 71–85, 2002). Treatment with cAMP (100 μM 8-cpt-cAMP plus 100 μM IBMX) stimulated ENaC-mediated Na+ absorption as well as Cl− secretion via cystic fibrosis transmembrane conductance regulator, which was characterized in α-toxin-permeabilized monolayers to have the anion selectivity sequence NO3− > Br− > Cl− > I−. With the use of FL-MDCK monolayers in which the basolateral membrane was permeabilized by nystatin, the ENaC conductance of the apical membrane [determined from the amiloride-sensitive short-circuit current (AS- Isc) driven by an apical-to-basolateral Na+ concentration gradient] was progressively inhibited by increasing the [Cl−] in the basolateral solution (and hence in the cytosol), but it was insensitive to the [Cl−] in the apical solution. This inhibitory effect of [Cl−]i occurred regardless of the presence or absence of net Cl− transport. However, from fluorometric measurements using the Cl−-sensitive dye 6-methoxy- N-(3-sulfopropyl)-quinolinium in intact FL-MDCK monolayers on permeable supports, cAMP, which activates both Na+ absorption and Cl− secretion, produced a decrease of [Cl−]i from 76 ± 14 to 36 ± 8 mM ( P = 0.03). Thus it might be expected that activation of Cl− secretion by cAMP would lead to stimulation rather than inhibition of ENaC. In the nystatin-treated monolayers, an increase in [Cl−]i from 15 to 145 mM decreased AS- Isc from 24.5 ± 1.0 to 10.2 ± 1.6 μA/cm2. This inhibition of ENaC could be attributed to nearly proportional decreases in the density of ENaC in the apical membrane from 1.91 ± 0.16 to 1.32 ± 0.17 fmol/cm2 and in the intrinsic channel activity (the average current per ENaC subunit) from 13.3 ± 1.2 to 8.2 ± 1.4 μA/fmol.

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Cyclic AMP-induced chloride permeability in the apical membrane of Necturus gallbladder epithelium.

Cited by 123 publications

References 36 publications

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Effects of theophylline, choleragen and loperamide on rabbit ileal fluid and electrolyte transport in vitro

Inhibition of ENaC by intracellular Cl⁻in an MDCK clone with high ENaC expression

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Cyclic AMP-induced chloride permeability in the apical membrane of Necturus gallbladder epithelium.

Cited by 123 publications

References 36 publications

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Effects of theophylline, choleragen and loperamide on rabbit ileal fluid and electrolyte transport in vitro

Inhibition of ENaC by intracellular Cl−in an MDCK clone with high ENaC expression

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Inhibition of ENaC by intracellular Cl⁻in an MDCK clone with high ENaC expression