Extracellular UTP stimulates electrogenic bicarbonate secretion across CFTR knockout gallbladder epithelium

2000 ◽  
Vol 279 (1) ◽  
pp. G132-G138 ◽  
Author(s):  
Lane L. Clarke ◽  
Matthew C. Harline ◽  
Lara R. Gawenis ◽  
Nancy M. Walker ◽  
John T. Turner ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Receptor Activation ◽  
Biliary Disease ◽  
Anion Conductance ◽  
Intracellular Ca ◽  
Ph Stat ◽  
Chamber Studies

The loss of cystic fibrosis transmembrane conductance regulator (CFTR)-mediated transepithelial HCO3 − secretion contributes to the pathogenesis of pancreatic and biliary disease in cystic fibrosis (CF) patients. Recent studies have investigated P2Y2 nucleotide receptor agonists, e.g., UTP, as a means to bypass the CFTR defect by stimulating Ca2+-activated Cl− secretion. However, the value of this treatment in facilitating transepithelial HCO3 − secretion is unknown. Gallbladder mucosae from CFTR knockout mice were used to isolate the Ca2+-dependent anion conductance during activation of luminal P2Y2receptors. In Ussing chamber studies, UTP stimulated a transient peak in short-circuit current ( I sc) that declined to a stable plateau phase lasting 30–60 min. The plateau I sc after UTP was Cl− independent, HCO3 − dependent, insensitive to bumetanide, and blocked by luminal DIDS. In pH stat studies, luminal UTP increased both I sc and serosal-to-mucosal HCO3 − flux ( J s→m) during a 30-min period. Substitution of Cl− with gluconate in the luminal bath to inhibit Cl−/HCO3 −exchange did not prevent the increase in J s→mand I sc during UTP. In contrast, luminal DIDS completely inhibited UTP-stimulated increases in J s→m and I sc. We conclude that P2Y2 receptor activation results in a sustained (30–60 min) increase in electrogenic HCO3 − secretion that is mediated via an intracellular Ca2+-dependent anion conductance in CF gallbladder.

A double-membrane model for urinary bicarbonate secretion

1985 ◽  
Vol 249 (4) ◽  
pp. F546-F552 ◽  
Author(s):  
D. L. Stetson ◽  
R. Beauwens ◽  
J. Palmisano ◽  
P. P. Mitchell ◽  
P. R. Steinmetz
Keyword(s):  
Channel Blocker ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Short Circuit Current ◽  
Ultrastructural Examination ◽  
Transport Pathway ◽  
Anion Conductance ◽  
Luminal Membrane ◽  
Disulfonic Stilbene ◽  
Ph Stat

To define the transport pathway for HCO-3 secretion (JHCO3) across the apical and basolateral membranes of turtle bladder, we examined the effects of cAMP, isobutylmethylxanthine (IBMX), the Cl- channel blocker 9-anthroic acid (9-AA), and the disulfonic stilbene DIDS (4,4'-diisothiocyanostilbene-2,2'-sulfonic acid) on the electroneutral and electrogenic components of JHCO3. Total JHCO3 was measured by pH stat titration of the mucosal compartment after Na+ absorption and H+ secretion were abolished by ouabain and a delta pH, respectively. Addition of cAMP or IBMX increased total JHCO3 and induced a short-circuit current (ISC), accounting for a large part of JHCO3; net Cl- absorption was reduced. Mucosal 9-AA inhibited the IBMX-induced electrogenic component of JHCO3, whereas mucosal DIDS inhibited the electroneutral component and acetazolamide reduced both. We suggest that HCO-3 is generated within the cell by a Na-independent primary active acid-base transport at the basolateral membrane (H+ extrusion into the serosal compartment). Cellular HCO-3 accumulation drives JHCO3 via a Cl-HCO3 exchanger at the luminal membrane. IBMX and cAMP activate a 9-AA-sensitive anion conductance parallel to the exchanger. The apparent reversal of the transport elements between the two cell membranes (compared with H+-secreting cells) led to an ultrastructural examination of the carbonic anhydrase-rich cells.

Expression of nucleotide-regulated Cl−currents in CF and normal mouse tracheal epithelial cell lines

2000 ◽  
Vol 279 (5) ◽  
pp. C1578-C1586 ◽  
Author(s):  
E. J. Thomas ◽  
S. E. Gabriel ◽  
M. Makhlina ◽  
S. P. Hardy ◽  
M. I. Lethem
Keyword(s):  
Epithelial Cell ◽  
Cell Lines ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
T Antigen ◽  
Epithelial Cell Lines ◽  
Chamber Studies ◽  
Cf Transmembrane Conductance Regulator

The dominant route for Cl− secretion in mouse tracheal epithelium is via Cl− channels different from the cystic fibrosis (CF) transmembrane conductance regulator (CFTR), the channel that is defective in CF. It has been proposed that the use of purinergic agonists to activate these alternative channels in human airways may be beneficial in CF. In the present study, two conditionally immortal epithelial cell lines were established from the tracheae of mice possessing the tsA58 T antigen gene, one of which [MTE18-(−/−)] was homozygous for a knockout of CFTR and the other [MTE7b-(+/−)] heterozygous for CFTR expression. In Ussing chamber studies, amiloride (10−4 M) and a cocktail of cAMP-activating agents (forskolin, IBMX, and dibutyryl cAMP) resulted in small changes in the short-circuit current ( I sc) and resistance of both cell lines, with larger increases in I scbeing elicited by ionomycin (10−6 M). Both cell lines expressed P2Y2 receptors and responded to the purinergic agonists ATP, UTP, and 5′-adenylylimidodiphosphate (10−4 M) with an increase in I sc. This response could be inhibited by DIDS and was abolished in the presence of Cl−-free Ringer solution. Reducing the mucosal Cl− concentration increased the response to UTP of both cell lines, with a significantly greater increase in MTE18-(−/−) cells. Pretreatment of these cells with thapsigargin caused a direct increase in I sc and inhibited the response to UTP. These data suggest that both cell lines express purinergic-regulated Cl− currents and may prove valuable tools in studying the properties of this pathway.

Agonists of protease-activated receptors 1 and 2 stimulate electrolyte secretion from mouse gallbladder

2007 ◽  
Vol 293 (1) ◽  
pp. G335-G346 ◽  
Author(s):  
Jacob G. Kirkland ◽  
Graeme S. Cottrell ◽  
Nigel W. Bunnett ◽  
Carlos U. Corvera
Keyword(s):  
Knockout Mice ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Gastrointestinal Diseases ◽  
Wild Type ◽  
Protease Activated Receptors ◽  
Intracellular Ca ◽  
Electrolyte Secretion ◽  
Homologous Desensitization

Cholecystitis is one of the most common gastrointestinal diseases. Inflammation induces the activation of proteases that can signal to cells by cleaving protease-activated receptors (PARs) to induce hemostasis, inflammation, pain, and repair. However, the distribution of PARs in the gallbladder is unknown, and their effects on gallbladder function have not been fully investigated. We localized immunoreactive PAR1 and PAR2 to the epithelium, muscle, and serosa of mouse gallbladder. mRNA transcripts corresponding to PAR1 and PAR2, but not PAR4, were detected by RT-PCR and sequencing. Addition of thrombin and a PAR1-selective activating peptide (TFLLRN-NH2) to the serosal surface of mouse gallbladder mounted in an Ussing chamber stimulated an increase in short-circuit current in wild-type but not PAR1 knockout mice. Similarly, serosally applied trypsin and PAR2 activating peptide (SLIGRL-NH2) increased short-circuit current in wild-type but not PAR2 knockout mice. Proteases and activating peptides strongly inhibited electrogenic responses to subsequent stimulation with the same agonist, indicating homologous desensitization. Removal of HCO3− ions from the serosal buffer reduced responses to thrombin and trypsin by >80%. Agonists of PAR1 and PAR2 increase intracellular Ca2+ concentration in isolated and cultured gallbladder epithelial cells. The COX-2 inhibitor meloxicam and an inhibitor of CFTR prevented the stimulatory effect of PAR1 but not PAR2. Thus PAR1 and PAR2 are expressed in the epithelium of the mouse gallbladder, and serosally applied proteases cause a HCO3− secretion. The effects of PAR1 but not PAR2 depend on generation of prostaglandins and activation of CFTR. These mechanisms may markedly influence fluid and electrolyte secretion of the inflamed gallbladder when multiple proteases are generated.

NH2-terminal modification of a channel-forming peptide increases capacity for epithelial anion secretion

2001 ◽  
Vol 280 (3) ◽  
pp. C451-C458 ◽  
Author(s):  
James R. Broughman ◽  
Kathy E. Mitchell ◽  
Roger L. Sedlacek ◽  
Takeo Iwamoto ◽  
John M. Tomich ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Glycine Receptor ◽  
Short Circuit Current ◽  
Disulfonic Acid ◽  
Α Subunit ◽  
Anion Secretion ◽  
Anion Conductance ◽  
Selective Channel

A synthetic, channel-forming peptide, derived from the α-subunit of the glycine receptor (M2GlyR), has been synthesized and modified by adding four lysine residues to the NH2 terminus (N-K4-M2GlyR). In Ussing chamber experiments, apical N-K4-M2GlyR (250 μM) increased transepithelial short-circuit current ( I sc) by 7.7 ± 1.7 and 10.6 ± 0.9 μA/cm2 in Madin-Darby canine kidney and T84 cell monolayers, respectively; these values are significantly greater than those previously reported for the same peptide modified by adding the lysines at the COOH terminus (Wallace DP, Tomich JM, Iwamoto T, Henderson K, Grantham JJ, and Sullivan LP. Am J Physiol Cell Physiol 272: C1672–C1679, 1997). N-K4-M2GlyR caused a concentration-dependent increase in I sc ( k [1/2] = 190 μM) that was potentiated two- to threefold by 1-ethyl-2-benzimidazolinone. N-K4-M2GlyR-mediated increases in I sc were insensitive to changes in apical cation species. Pharmacological inhibitors of endogenous Cl− conductances [glibenclamide, diphenylamine-2-dicarboxylic acid, 5-nitro-2-(3-phenylpropylamino)benzoic acid, 4,4′-dinitrostilben-2,2′-disulfonic acid, indanyloxyacetic acid, and niflumic acid] had little effect on N-K4-M2GlyR-mediated I sc. Whole cell membrane patch voltage-clamp studies revealed an N-K4-M2GlyR-induced anion conductance that exhibited modest outward rectification and modest time- and voltage-dependent activation. Planar lipid bilayer studies yielded results indicating that N-K4-M2GlyR forms a 50-pS anion conductance with a k [1/2] for Cl−of 290 meq. These results indicate that N-K4-M2GlyR forms an anion-selective channel in epithelial monolayers and shows therapeutic potential for the treatment of hyposecretory disorders such as cystic fibrosis.

Na+/Ca2+ exchange regulates Ca2+-dependent duodenal mucosal ion transport and HCO3− secretion in mice

2005 ◽  
Vol 288 (3) ◽  
pp. G457-G465 ◽  
Author(s):  
Hui Dong ◽  
Zachary M. Sellers ◽  
Anders Smith ◽  
Jimmy Y. C. Chow ◽  
Kim E. Barrett
Keyword(s):  
Western Blot ◽  
Ion Transport ◽  
Muscarinic Receptors ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Duodenal Mucosa ◽  
Ussing Chambers ◽  
Intracellular Ca ◽  
Ph Stat ◽  
Stimulation Of

Stimulation of muscarinic receptors in duodenal mucosa raises intracellular Ca2+, which regulates ion transport, including HCO3− secretion. However, the underlying Ca2+ handling mechanisms are poorly understood. The aim of the present study was to determine whether Na+/Ca2+ exchanger (NCX) plays a role in the regulation of duodenal mucosal ion transport and HCO3− secretion by controlling Ca2+ homeostasis. Mouse duodenal mucosa was mounted in Ussing chambers. Net ion transport was assessed as short-circuit current ( Isc), and HCO3− secretion was determined by pH-stat. Expression of NCX in duodenal mucosae was analyzed by Western blot, and cytosolic Ca2+ in duodenocytes was measured by fura 2. Carbachol (100 μM) increased Isc in a biphasic manner: an initial transient peak within 2 min and a later sustained plateau starting at 10 min. Carbachol-induced HCO3− secretion peaked at 10 min. 2-Aminoethoxydiphenylborate (2-APB, 100 μM) or LiCl (30 mM) significantly reduced the initial peak in Isc by 51 or 47%, respectively, and abolished the plateau phase of Isc without affecting HCO3− secretion induced by carbachol. Ryanodine (100 μM), caffeine (10 mM), and nifedipine (10 μM) had no effect on either response to carbachol. In contrast, nickel (5 mM) and KB-R7943 (10–30 μM) significantly inhibited carbachol-induced increases in duodenal mucosal Isc and HCO3− secretion. Western blot analysis showed expression of NCX1 proteins in duodenal mucosae, and functional NCX in duodenocytes was demonstrated in Ca2+ imaging experiments where Na+ depletion elicited Ca2+ entry via the reversed mode of NCX. These results indicate that NCX contributes to the regulation of Ca2+-dependent duodenal mucosal ion transport and HCO3− secretion that results from stimulation of muscarinic receptors.

T84 cells: anion selectivity demonstrates expression of Cl- conductance affected in cystic fibrosis

1992 ◽  
Vol 262 (3) ◽  
pp. C555-C562 ◽  
Author(s):  
C. L. Bell ◽  
P. M. Quinton
Keyword(s):  
Cystic Fibrosis ◽  
Short Circuit ◽  
Membrane Surface ◽  
Short Circuit Current ◽  
Basal Membrane ◽  
Apical Surface ◽  
T84 Cells ◽  
Anion Conductance ◽  
Anion Selectivity ◽  
Cl Conductance

The T84 cell line possesses an adenosine 3',5'-cyclic monophosphate (cAMP)-activated Cl- conductance and expresses high levels of the cystic fibrosis (CF) gene product, implicating it as a good model for CF research. To evaluate whether T84 Cl- conductance properties are consistent with those described in CF target epithelial, we used transepithelial measurements (verified by selective permeabilization of the basal membrane) to determine the apparent anion selectivity properties of the apical and basolateral membranes of stimulated and unstimulated T84 cells. Unstimulated epithelial cells were almost electrically inert, having a low transepithelial voltage (Vt; -6 mV, apical surface negative), a small equivalent short-circuit current (Isc,(eq.) 2.2 microA/cm2), a very high transepithelial resistance (Rt; 2,500 omega.cm2), and poor anion permselectivity properties at both membrane surfaces (0.8 less than PX/PCl- less than 1.1), where X is NO3-, Br-, I-, or gluconate. When stimulated with forskolin (10(-6) M), Vt increased 8-fold, Isc(eq) increased 30-fold, Rt fell to one-third of unstimulated values, and the apical surface became highly anion selective, i.e., NO3- (1.4) greater than Br- (1.2) greater than Cl- (1.0) greater than I- (0.7) greater than gluconate (0.0), where numbers in parentheses are PX/PCl-. I- was less permeable than Cl- and probably directly inhibits the anion conductance, since Rt was substantially greater after I- substitution than after substitution with the impermeable anion gluconate. Bumetanide (10(-4) M) significantly attenuated the response of Vt to anion substitutions at the basal membrane surface, indicating that the effects of substitution were predominantly on the Na(+)-K(+)-2Cl- cotransporter.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Regulatory domain phosphorylation to distinguish the mechanistic basis underlying acute CFTR modulators

2011 ◽  
Vol 301 (4) ◽  
pp. L587-L597 ◽  
Author(s):  
Louise C. Pyle ◽  
Annette Ehrhardt ◽  
Lisa High Mitchell ◽  
LiJuan Fan ◽  
Aixia Ren ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
High Throughput Screening ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Regulatory Domain ◽  
Thyroid Cells ◽  
Binding Domains ◽  
Mechanistic Basis ◽  
Rat Thyroid

Modulator compounds intended to overcome disease-causing mutations in the cystic fibrosis transmembrane conductance regulator ( CFTR) show significant promise in clinical testing for cystic fibrosis. However, the mechanism(s) of action underlying these compounds are not fully understood. Activation of CFTR ion transport requires PKA-regulated phosphorylation of the regulatory domain (R-D) and dimerization of the nucleotide binding domains. Using a newly developed assay, we evaluated nine compounds including both CFTR potentatiators and activators discovered via various high-throughput screening strategies to acutely augment CFTR activity. We found considerable differences in the effects on R-D phosphorylation. Some (including UCCF-152) stimulated robust phosphorylation, and others had little effect (e.g., VRT-532 and VX-770). We then compared CFTR activation by UCCF-152 and VRT-532 in Ussing chamber studies using two epithelial models, CFBE41o− and Fischer rat thyroid cells, expressing various CFTR forms. UCCF-152 activated wild-type-, G551D-, and rescued F508del-CFTR currents but did not potentiate cAMP-mediated CFTR activation. In contrast, VRT-532 moderately activated CFTR short-circuit current and strongly potentiated forskolin-mediated current. Combined with the result that UCCF-152, but not VRT-532 or VX-770, acts by increasing CFTR R-D phosphorylation, these findings indicate that potentiation of endogenous cAMP-mediated activation of mutant CFTR is not due to a pathway involving augmented R-D phosphorylation. This study presents an assay useful to distinguish preclinical compounds by a crucial mechanism underlying CFTR activation, delineates two types of compound able to acutely augment CFTR activity (e.g., activators and potentiators), and demonstrates that a number of different mechanisms can be successfully employed to activate mutant CFTR.

scholarly journals Assessment of Distinct Electrophysiological Parameters in Rectal Biopsies for the Choice of the Best Diagnosis/Prognosis Biomarkers for Cystic Fibrosis

2020 ◽  
Vol 11 ◽  
Author(s):  
Iris A. L. Silva ◽  
Aires Duarte ◽  
Fernando A. L. Marson ◽  
Raquel Centeio ◽  
Tereza Doušová ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Clinical Features ◽  
Ex Vivo ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Predictive Biomarker ◽  
Sweat Chloride ◽  
Best Parameter ◽  
Rectal Biopsies

Most cases of Cystic Fibrosis (CF) are diagnosed early in life. However, people with atypical CF forms pose diagnosis dilemmas, requiring laboratory support for diagnosis confirmation/exclusion. Ex vivo analysis of fresh rectal biopsies by Ussing chamber has been the best discriminant biomarker for CF diagnosis/prognosis so far. Here we aimed to evaluate different electrophysiological parameters from Ussing chamber analysis of rectal biopsies from people with CF (PwCF) to establish the one with highest correlations with clinical features as the best CF diagnosis/prognosis biomarker. We analyzed measurements of CFTR-mediated Cl– secretion in rectal biopsies from 143 individuals (∼592 biopsies), the largest cohort so far analyzed by this approach. New parameters were analyzed and compared with the previous biomarker, i.e., the IBMX (I)/Forskolin (F)/Carbachol (C)-stimulated short-circuit current (I’sc–I/F/C). Correlations with clinical features showed that the best parameter corresponded to voltage measurements of the I/F + (I/F/CCH) response (VI/F+I/F/C), with higher correlations vs. I’sc–I/F/C for: sweat chloride (59 vs. 52%), fecal elastase (69 vs. 55%) and lung function, measured by FEV1 (27 vs. 20%). Altogether data show that VI/F+I/F/C is the most sensitive, reproducible, and robust predictive biomarker for CF diagnosis/prognosis effectively discriminating classical, atypical CF and non-CF groups.

Cholinergic ion secretion in human colon requires coactivation by cAMP

1998 ◽  
Vol 275 (6) ◽  
pp. G1274-G1281 ◽  
Author(s):  
M. Mall ◽  
M. Bleich ◽  
M. Schürlein ◽  
J. Kühr ◽  
H. H. Seydewitz ◽  
...  
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Human Colon ◽  
Intracellular Camp ◽  
Camp Production ◽  
Ion Secretion ◽  
Negative Current ◽  
Intracellular Ca ◽  
Second Messenger Pathways

Cl−secretion in the colon can be activated by an increase of either intracellular Ca2+ or cAMP. In this study we examined a possible interdependence of the two second-messenger pathways in human colonic epithelium. When measured in a modified Ussing chamber, carbachol (CCH; 100 μmol/l, basolateral), via an increase in cytosolic Ca2+concentration ([Ca2+]i), activated a transient lumen-negative equivalent short-circuit current ( I sc) [change (Δ) in I sc = −79.4 ± 7.5 μA/cm2]. Previous studies indicated that intracellular Ca2+ directly acts on basolateral K+ channels, thus enhancing driving force for luminal Cl− exit. Increased intracellular cAMP (by basolateral addition of 100 μmol/l IBMX and 1 μmol/l forskolin) activated a sustained lumen-negative current (Δ I sc = −42.4 ± 7.2 μA/cm2) that was inhibited by basolateral trans-6-cyano-4-( N-ethylsulfonyl- N-methylamino)-3-hydroxy-2,2-dimethyl&2-chromane (10 μmol/l), a blocker of KvLQT1 channels. In the presence of elevated cAMP, the CCH-activated currents were augmented (Δ I sc = 167.7 ± 32.7 μA/cm2), suggesting cooperativity of the Ca2+- and cAMP-mediated responses. Inhibition of endogenous cAMP production by indomethacin (10 μmol/l) significantly reduced CCH-activated currents and even reversed the polarity in 70% of the experiments. The transient lumen-positive I sc was probably due to activation of apical K+channels because it was blocked by luminal Ba2+ (5 mmol/l) and tetraethylammonium (10 mmol/l). In the presence of indomethacin (10 μmol/l, basolateral), an increase of cAMP activated a sustained negative I sc. Under these conditions, CCH induced a large further increase in lumen-negative I sc(Δ I sc = −100.0 ± 21.0 μA/cm2). We conclude that CCH acting via [Ca2+]ican induce Cl− secretion only in the presence of cAMP, i.e., when luminal Cl− channels are already activated. The activation of a luminal and basolateral K+ conductance by CCH may be essential for transepithelial KCl secretion in human colon.

Interleukin-13 induces a hypersecretory ion transport phenotype in human bronchial epithelial cells

2002 ◽  
Vol 282 (2) ◽  
pp. L226-L236 ◽  
Author(s):  
Henry Danahay ◽  
Hazel Atherton ◽  
Gareth Jones ◽  
Robert J. Bridges ◽  
Christopher T. Poll
Keyword(s):  
Epithelial Cells ◽  
Ion Transport ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Fluid Secretion ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Anion Conductance

Interleukin (IL)-13 has been associated with asthma, allergic rhinitis, and chronic sinusitis, all conditions where an imbalance in epithelial fluid secretion and absorption could impact upon the disease. We have investigated the effects of IL-13 on the ion transport characteristics of human bronchial epithelial cells cultured at an apical-air interface. Ussing chamber studies indicated that 48 h pretreatment with IL-13 or IL-4 significantly reduced the basal short-circuit current ( I sc) and inhibited the amiloride-sensitive current by >98%. Furthermore, the I scresponses were increased by more than six- and twofold over control values when stimulated with UTP or forskolin, respectively, after cytokine treatment. The IL-13-enhanced response to UTP/ionomycin was sensitive to bumetanide and DIDS and was reduced in a low-chloride, bicarbonate-free solution. Membrane permeablization studies indicated that IL-13 induced the functional expression of an apical Ca2+-activated anion conductance and that changes in apical or basolateral K+ conductances could not account for the increased I sc responses to UTP or ionomycin. The results indicate that IL-13 converts the human bronchial epithelium from an absorptive to a secretory phenotype that is the result of loss of amiloride-sensitive current and an increase in a DIDS-sensitive apical anion conductance.

Sign in / Sign up

Export Citation Format

Share Document