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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have reported that in the rabbit cortical collecting duct (CCD) we can identify electrophysiologically three distinct cell types; the collecting duct (CD) cell and the alpha- and beta-intercalated (IC) cell. To further characterize the Cl- transport properties of each cell type, we examined the interaction between Cl- and other halogens or SCN- in the isolated and perfused CCD by intracellular microelectrode impalement. The rapid depolarization of the basolateral membrane potential (VB) caused by replacement of bath Cl- with each anion revealed that the sequences of apparent halogen selectivity for the basolateral Cl- conductance were similar in all three cell types. The ranking of Cl- > Br- > F- > I- corresponds to the sequence 5 of Eisenman's series, indicating "strong" interaction of the anions with the selectivity site. The basolateral Cl- conductance of these three cell types may share common characteristics, although I- permeability is less in IC cells than in CD cells. Hyperpolarization of the basolateral membrane of the beta-IC cell upon reduction of luminal Cl- reflects alterations in either Cl- entry across the apical membrane, or Cl- exit across the basolateral membrane, or both. Luminal Cl- replacement with each anion showed that the sequence of the hyperpolarization of the basolateral membrane was I- >> cyclamate = SCN- > F- > Br-, suggesting that I-inhibits either apical Cl- entry or basolateral Cl- exit. On the other hand, in the CD cell reduction of the perfusate Cl- by replacement with each anion caused the basolateral membrane to hyperpolarize with a different ranking: cyclamate = F- > I- = SCN- > Br-.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction of Cl- and other halogens with Cl- transport systems in rabbit cortical collecting duct. 144 75

The renal medullary collecting duct (MCD) secretes protons into its lumen and HCO3 into its basolateral space. Basolateral HCO3 transport is thought to occur via Cl/HCO3 exchange. To further characterize this Cl/HCO3 exchange process, intracellular pH (pHi) regulation was monitored in freshly prepared rabbit outer MCD cells. Cells were separated by protease digestion and purified by Ficoll gradient centrifugation. pHi was estimated fluorometrically using the entrapped intracytoplasmic pH indicator, 6-carboxyfluorescein. Cells were preincubated in bicarbonate-containing solutions and then abruptly diluted into bicarbonate-free media. The MCD cell pHi response to abrupt removal of CO2/HCO3 included an initial alkalinization due to rapid CO2 efflux, followed by an acidification due to HCO3 efflux and a gradual recovery to the resting pHi of 7.24 +/- 0.06 partly due to the action of a plasma membrane H+-ATPase. The initial alkalinization required a CO2/HCO3 gradient and did not occur in the presence of acetazolamide. The acidification phase required intracellular HCO3 and extracellular Cl, which was consistent with a Cl/HCO3 exchange. MCD HCO3 efflux exhibited saturable kinetics for extracellular Cl, with a Michaelis constant (Km) of 29.9 +/- 7.7 mM. HCO3 efflux also exhibited preference for halides over NO3, SCN, and gluconate, and striking sensitivity to disulfonic stilbene and acetazolamide inhibition, with an apparent K1 of 5 X 10(-7) M for DIDS. The final pHi recovery required intracellular ATP, which indicated that Cl/HCO3 and H+-ATPase activities are present in the same cells in these suspensions. The results provide direct evidence for MCD Cl/HCO3 exchange and describe some of the properties of this transport process.
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PMID:Intracellular pH regulation in rabbit renal medullary collecting duct cells. Role of chloride-bicarbonate exchange. 287 Oct 45

The chloride conductance of inner medullary collecting duct cells (mIMCD-3 cell line) has been investigated using the whole cell configuration of the patch clamp technique. Seventy-seven percent of cells were chloride selective when measured with a NaCl-rich bathing solution and a TEACl-rich pipette solution. Seventy-five percent of chloride-selective cells (90/144) had whole cell currents which exhibited an outwardly-rectifying (OR) current-voltage (I/V) relationship, while the remaining cells exhibited a linear (L) I/V relationship. The properties of the OR and L chloride currents were distinct. OR currents (mean current densities at +/- 60 mV of 66 +/- 5 pA/pF and 44 +/- 3 pA/pF), were time- and voltage-independent with an anion selectivity (from calculated permeability ratios) of SCN- (2.3), NO3- (1.8), ClO4- (1.7), Br- (1.7), I- (1.6), Cl- (1.0), HCO3- (0.5), gluconate- (0.2). Bath additions of NPPB, flufenamate, glibenclamide (all 100 microM) and DIDS (500 microM) produced varying degrees of block of OR currents with NPPB being the most potent (IC50 of approximately 50 microM) while DIDS was the least effective. Linear chloride currents had similar current densities to the OR chloride currents and were also time- and voltage-independent. The anion selectivity sequence was SCN- (2.5), NO3- (1.9), Br- (1.4), I- (1.1), Cl- (1.0), ClO4- (0.5), HCO3- (0.5), gluconate- (0.3). In contrast to the OR conductance, glibenclamide was the most potent and DIDS the least potent blocker of L currents. An IC50 of > 100 microM was observed for NPPB block. Neither OR of L chloride currents were affected by acutely or chronically increased intracellular cAMP and were not affected when intracellular Ca2+ levels were increased or decreased. The molecular identity and physiological role of OR and linear currents in mIMCD-3 cells are discussed.
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PMID:Characterization of whole cell chloride conductances in a mouse inner medullary collecting duct cell line mIMCD-3. 882 25

Whole cell recordings were performed on rat inner medullary collecting duct (IMCD) cells in primary culture. With 140 mmol/l CsCl in bath and pipette we find within 10 min a 60-fold increase in membrane conductance from 0.02 +/- 0.003 to 1.2 +/- 0.1 nS/pF when bath osmolarity is decreased from 600 to 500 mosmol/l. The effect is due to the activation of an outwardly rectifying anion conductance with the anion selectivity SCN- > I- > NO-3 > Br- > Cl- > F- > isethionate > gluconate > or = aspartate > or = glutamate. A relative permeability of the organic osmolyte taurine to Cl- (Ptaurine: PCl-) of 0.15 was detected. With taurine in pipette and bath, the channel exhibits a nearly identical activation and sensitivity profile to a variety of anion channel blockers as under symmetrical Cl- conditions. Furthermore, the 50% inhibitory concentration value for the effect of 5-nitro-2-(3-phenylpropylamino)benzoate on both currents is virtually identical. We conclude that hypotonic stress increases the anion conductance of rat IMCD cells and that this anion conductance mediates taurine efflux.
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PMID:Taurine permeation through swelling-activated anion conductance in rat IMCD cells in primary culture. 885 11

In the present study we used whole-cell patch clamp recordings to investigate swelling-activated Cl-currents (ICl-swell) in M-1 mouse cortical collecting duct (CCD) cells. Hypotonic cell swelling reversibly increased the whole-cell Cl- conductance by about 30-fold. The I-V relationship was outwardly-rectifying and ICl-swell displayed a characteristic voltage-dependence with relatively fast inactivation upon large depolarizing and slow activation upon hyperpolarizing voltage steps. Reversal potential measurements revealed a selectivity sequence SCN- > I- > Br- > Cl- > > gluconate. ICl-swell was inhibited by tamoxifen, NPPB (5-nitro-2(3-phenylpropylamino)-benzoate), DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid), flufenamic acid, niflumic acid, and glibenclamide, in descending order of potency. Extracellular cAMP had no significant effect. ICl-swell was Ca2+ independent, but current activation depended on the presence of a high-energy gamma-phosphate group from intracellular ATP or ATP gamma S. Moreover, it depended on the presence of intracellular Mg2+ and was inhibited by staurosporine, which indicates that a phosphorylation step is involved in channel activation. Increasing the cytosolic Ca2+ concentration by using ionomycin stimulated Cl- currents with a voltage dependence different from that of ICl-swell. Analysis of whole-cell current records during early onset of ICl-swell and during final recovery revealed discontinuous step-like changes of the whole-cell current level which were not observed under nonswelling conditions. A single-channel I-V curve constructed using the smallest resolvable current transitions detected at various holding potentials and revealed a slope conductance of 55, 15, and 8 pS at +120, 0, and -120 mV, respectively. The larger current steps observed in these recordings had about 2, 3, or 4 times the size of the putative single-channel current amplitude, suggesting a coordinated gating of several individual channels or channel subunits. In conclusion we have functionally characterized ICl-swell in M-1 CCD cells and have identified the underlying single channels in whole-cell current recordings.
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PMID:Cell swelling activates ATP-dependent voltage-gated chloride channels in M-1 mouse cortical collecting duct cells. 888 62

Confluent M-1 mouse cortical collecting duct (CCD) cells express highly selective low-conductance amiloride-sensitive Na+ channels (B. Letz, A. Ackermann, C. M. Canessa, B. C. Rossier, and C. Korbmacher, J. Membr. Biol. 148: 129-143, 1995). Here we investigated the effect of forskolin on membrane voltage and whole cell currents of confluent M-1 cells using the patch-clamp technique. Forskolin (1 microM) reduced the hyperpolarization in response to amiloride (10 microM) from 17 to 4 mV and decreased the amiloride-sensitive Na+ inward currents from 81 to 26 pA. Furthermore, forskolin increased the hyperpolarization caused by changing from an apical low-Cl- solution (9 mM) to a high-Cl- solution (149 mM) from 11 to 30 mV and increased the magnitude of the inward current changes induced by alternating between high-Cl- and low-Cl- solutions from 25 to 138 pA. This demonstrates that forskolin stimulates an apical Cl- conductance. Anion substitution experiments revealed a permeability sequence SCN- > Br- > Cl- > I- >> gluconate. This suggests that the stimulated channels are cystic fibrosis transmembrane conductance regulator (CFTR)-like Cl- channels. 3-Isobutyl-1-methylxanthine and 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate mimicked the effects of forskolin, whereas 1,9-dideoxyforskolin had no effect. We conclude that, in addition to amiloride-sensitive Na+ channels, CFTR-like Cl- channels are present in the apical membrane of confluent M-1 cells. An increase in intracellular adenosine 3',5'-cyclic monophosphate (cAMP) activates these Cl- channels and concurrently reduces the activity of the Na+ channels. This reciprocal regulation by cAMP suggests that the channels are functionally coupled.
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PMID:cAMP stimulates CFTR-like Cl- channels and inhibits amiloride-sensitive Na+ channels in mouse CCD cells. 912 10

Cl- currents were observed under whole cell clamp conditions in cells of the rat cortical collecting duct (CCD), connecting tubule (CNT), and thick ascending limb of Henle's loop (TALH). These currents were much larger in intercalated cells compared with principal cells of the CCD and were also larger in the TALH and in the CNT compared with the CCD. The conductance had no strong voltage dependence, and steady-state currents were similar in inward and outward directions with similar Cl- concentrations on both sides of the membrane. Current transients were observed, particularly at low Cl- concentrations, which could be explained by solute depletion and concentration in fluid layers next to the membrane. The currents had a remarkable selectivity among anions. Among halides, Br- and F- conductances were only 15% of that of Cl-, and I- conductance was immeasurably small. SCN- and OCN- conductances were approximately 50%, and aspartate, glutamate, and methanesulfonate conductance was approximately 5% that of Cl-. No conductance could be measured for any other anion tested, including NO3-, HCO3-, formate, acetate, or isethionate; NO3- and I- appeared to block the channels weakly. Conductances were diminished by lowering the extracellular pH to 6.4. The properties of the conductance fit best with those of the cloned renal anion channel ClC-K2 and likely reflect the basolateral Cl- conductances of the cells of these nephron segments.
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PMID:Cl- channels of the distal nephron. 1716 96