Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • K+ conductance  (9)
  • 1
    Electronic Resource
    Electronic Resource
    Effects of ouabain and temperature on cell membrane potentials in isolated perfused straight proximal tubules of the mouse kidney (1986)
    Springer
    Pflügers Archiv 407 (1986), S. 252-257 
    Details
    ISSN: 1432-2013
    Keywords: Proximal tubule ; Kidney ; K+ conductance ; Cell membrane potential ; Ouabain temperature ; Phlorizin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In isolated perfused segments of the mouse proximal tubule, the potential difference across the basolateral cell membrane (PDbl) was determined with conventional microelectrodes. Under control conditions with symmetrical solutions it amounted to −62±1 mV (n=118). The potential difference across the epithelium (PDte) was −1.7±0.1 mV (n=45). Transepithelial resistance amounted to 1.82±0.09 kΩ cm (n=28), corresponding to 11.4±0.6 Ω cm2. Increasing bath potassium concentration from 5 to 20 mmol/l depolarized PDbl by +24±1 mV (n=103), and PDte by +1.6±0.1 mV (n=19). Thus, the basolateral cell membrane is preferably conductive to potassium. Rapid cooling of the bath perfusate from 38°C to 10°C led to a transient hyperpolarization of PDbl from −60±1 to −65±1 mV (n=21) within 40 s followed by gradual depolarization by +18±1% (n=14) within 5 min. The transepithelial resistance increased significantly from 1.78±0.11 kΩ cm to 2.20±0.21 kΩ cm (n=15). Rapid rewarming of the bath to 38°C caused a depolarization from −61±2 mV (n=17) to −43±2 mV (n=16) within 15 s followed by a repolarization to −59±2 mV (n=10) within 40 s. Ouabain invariably depolarized PDbl. During both, sustained cooling or application of ouabain, the sensitivity of PDbl to bath potassium concentration decreased in parallel to PDbl pointing to a gradual decrease of potassium conductance. Phlorizin hyperpolarized the cell membrane from −59±2 to −66±1 mV (n=13), virtually abolished the transient hyperpolarization under cooling, and significantly reduced the depolarization after rewarming from +17±2 mV (n=16) to +9±3 mV (n=9). The present data indicate that the contribution of peritubular potassium conductance to the cell membrane conductance decreases following inhibition of basolateral (Na++K+)-ATPase. Apparently, cooling from 37° to 10°C does not only reduce (Na−+K+)-ATPase activity but in addition luminal sodium uptake mechanisms such as the sodium glucose cotransporter. As a result, cooling leads to an initial hyperpolarization of the cell followed by depolarization only after some delay.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585299
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Electrophysiological study of transport systems in isolated perfused pancreatic ducts: properties of the basolateral membrane (1988)
    Springer
    Pflügers Archiv 411 (1988), S. 58-68 
    Details
    ISSN: 1432-2013
    Keywords: Pancreas ; Isolated perfused ducts ; HCO 3 − transport ; K+ conductance ; (Na++K+)-ATPase ; Na+/H+ antiport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to study the mechanism of pancreatic HCO 3 − transport, a perfused preparation of isolated intra-and interlobular ducts (i.d. 20–40 μm) of rat pancreas was developed. Responses of the epithelium to changes in the bath ionic concentration and to addition of transport inhibitors was monitored by electrophysiological techniques. In this report some properties of the basolateral membrane of pancreatic duct cells are described. The transepithelial potential difference (PDte) in ducts bathed in HCO 3 − -free and HCO 3 − -containing solution was −0.8 and −2.6 mV, respectively. The equivalent short circuit current (Isc) under similar conditions was 26 and 50 μA·cm−2. The specific transepithelial resistance (Rte) was 88 Ωcm2. In control solutions the PD across the basolateral membrane (PDbl) was −63±1 mV (n=314). Ouabain (3 mmol/l) depolarized PDbl by 4.8±1.1 mV (n=6) within less than 10 s. When the bath K+ concentration was increased from 5 to 20 mmol/l, PDbl depolarized by 15.9±0.9 mV (n=50). The same K+ concentration step had no effect on PDbl if the ducts were exposed to Ba2+, a K+ channel blocker. Application of Ba2+ (1 mmol/l) alone depolarized PDbl by 26.4±1.4 mV (n=19), while another K+ channel blocker TEA+ (50 mmol/l) depolarized PDbl only by 7.7±2.0 mV (n=9). Addition of amiloride (1 mmol/l) to the bath caused 3–4 mV depolarization of PDbl. Furosemide (0.1 mmol/l) and SITS (0.1 mmol/l) had no effect on PDbl. An increase in the bath HCO 3 − concentration from 0 to 25 mmol/l produced fast and sustained depolarization of PDbl by 8.5±1.0 mV (n=149). It was investigated whether the effect of HCO 3 − was due to a Na++-dependent transport mechanism on the basolateral membrane, where the ion complex transferred into the cell would be positively charged, or whether it was due to decreased K+ conductance caused by lowered intracellular pH. Experiments showed that the HCO 3 − effect was present even when the bath Na+ concentration was reduced to a nominal value of 0 mmol/l. Similarly, the HCO 3 − effect remained unchanged after Ba2+ (5 mmol/l) was added to the bath. The results indicate that on the basolateral membrane of duct cells there is a ouabain sensitive (Na++K+)-ATPase, a Ba2+ sensitive K+ conductance and an amiloride sensitive Na+/H+ antiport. The HCO 3 − effect on PDbl is most likely due to rheogenic anion exit across the luminal membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581647
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Effect of bicarbonate on potassium conductance of isolated perfused rat pancreatic ducts (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 76-83 
    Details
    ISSN: 1432-2013
    Keywords: Pancreas ; Ducts ; K+ conductance ; Barium ; Bicarbonate ; Cell membrane resistances ; Secretin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to investigate the role of the K+ conductance in unstimulated and stimulated pancreatic ducts and to see how it is affected by provision of exogenous HCO 3 − /CO2. For this purpose we have applied electrophysiological techniques to perfused pancreatic ducts, which were dissected from rat pancreas. The basolateral membrane potential PDbl of unstimulated duct cells was between −60mV and −70mV, and the cells had a relatively large K+ conductance in the basolateral membrane as demonstrated by (a) 20–22 mV depolarization of PDbl in response to increase in bath K+ concentration from 5 mmol/l to 20mmol/l and (b) the effect of a K+ channel blocker, Ba2+ (5 mmol/l), which depolarized PDbl by 30–40mV. These effects on unstimulated ducts were relatively independent of bath HCO 3 − /CO2. The luminal membrane seemed to have no significant K+ conductance. Upon stimulation with secretin or dibutyryl cyclic AMP, PDbl depolarized to about −35 mV in the presence of HCO 3 − /CO2. Notably, the K+ conductance in the stimulated ducts was now only apparent in the presence of exogenous HCO 3 − /CO2 in the bath solutions. Upon addition of Ba2+, PDbl depolarized by 13±1 mV (n=7), the fractional resistance of the basolateral membrane, FRbl increased from 0.66 to 0.78 (n=6), the specific transepithelial resistance, R te, increased from 52±13 Ω cm2 to 59±15 Ω cm2 (n=11), and the whole-cell input resistance, R c, measured with double-barrelled electrodes, increased from 20 MΩ to 26 MΩ (n=3). These results are consistent with Ba2+ inhibition of the K+ conductance. Following removal of exogenous HCO 3 − /CO2 in the same ducts, stimulation led to a larger depolarization on PDbl to about −25 mV, and Ba2+ had a smaller effect on PDbl and no significant effect on the resistances. The individual resistances in the duct epithelium were estimated from equivalent circuit analysis. The luminal membrane resistance, R 1 decreased from about 2000 Ω cm2 to 80 Ω cm2 upon stimulation. The basolateral membrane resistance, R bl, remained at 90–120 Ω cm2, and the paracellular shunt resistance, R s, at 50–80 Ω cm2. Ba2+ increased R bl of stimulated ducts to about 200 Ω cm2, an effect present only if the ducts were provided with exogenous HCO 3 − /CO2. Taken together, the present results indicate that the basolateral K+ conductance of pancreatic ducts is sensitive to exogenous HCO 3 − /CO2, i.e. without HCO 3 − /CO2 the conductance becomes very low although the ducts are undergoing stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373750
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Potassium conductance of smooth muscle cells from rabbit aorta in primary culture (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 57-68 
    Details
    ISSN: 1432-2013
    Keywords: Vascular smooth muscle cell ; K+ conductance ; Big Ca2+-dependent K+ channel ; Patch clamp ; Verapamil ; Protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vascular smooth muscle cells were obtained from rabbit aorta and were studied in primary culture on days 1–7 after seeding with electrophysiological techniques. In impalement experiments a mean membrane potential difference (PD) of −50±0.3 mV (n=387) was obtained with Ringer-type solution in the bath. PD was depolarized by 6±0.3 mV (n=45) and 16±2 mV (n= 5) when the bath K+ concentration was increased from the control value of 3.6 mmol/l to 13.6 and 23.6 mmol/l, respectively. Ba2+ (0.1–1 mmol/l) depolarized PD. Tetraethylammonium (TEA, 10 mmol/l) depolarized PD only slightly but significantly. Verapamil (0.1 mmol/l) and charybdotoxin (10 nmol/l) had no effect on PD. The conductance properties of these cells were further examined with the patch-clamp technique. K+ channels were spontaneously present in cell-attached patches. When the pipette was filled with 145 mmol/l KCl, a mean conductance (g K) of 209.6±4.6 mV (n=17) was read from the current/voltage curves at a clamp voltage (V c) of 0 mV. After excision K+ channels were found in 129 patches with inside-out and in 50 with outside-out configuration. With KCl on one and NaCl on the other side the mean g K at a V c of 0 mV was 134.6±3.9 pS (n=179). The mean permeability was 0.89±0.03×10−12 cm3/s. With symmetrical KCl solution the mean g K was 227±6 pS (n=17). The conductance sequence was g K≫ g Rb= g Cs=g Na=0. TEA blocked dose-dependently only from the outside.(1–10 mmol/l). Lidocaine (5 mmol/l) quinidine (0.01–1 mmol/l) and quinine (0.01–1 mmol/l) blocked from both sides. Charybdotoxin (0.5–5 nmol/l) blocked only from the extracellular side. Ba2+ blocked from the cytosolic side and the inhibition was increased by depolarization and reduced by hyperpolarization. At a V c of 0 mV a half-maximal inhibition (IC50) of 2 μmol/l was obtained. Verapamil and diltiazem blocked from both sides, verapamil with an IC50 of 2 μmol/l and diltiazem with an IC50 of 10 μmol/l. The open probability of this channel was increased by Ca2+ on the cytosolic side at activities 〉 0.1 μmol/l. Half-maximal activation occurred at Ca2+ activities exceeding 1 μmol/l. The present data indicate that the vascular smooth muscle cells of rabbit aorta in primary culture possess a K+ conductance. In excised patches only a maxi K+ channel was detected. This channel has properties different from the macroscopic K+ conductance. Hence, it is likely that the K+ conductance of the intact cell is dominated by yet another and thus far not detected K+ channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373748
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Ca2+- and swelling-induced activation of ion conductances in bronchial epithelial cells (1994)
    Springer
    Pflügers Archiv 428 (1994), S. 597-603 
    Details
    ISSN: 1432-2013
    Keywords: Cl− conductance ; K+ conductance ; ATP ; Bradykinin ; Histamine ; Bronchial epithelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was performed to examine Ca2+-dependent and cell-swelling-induced ion conductances in a polarized bronchial epithelial cell line (16HBE14o-). Whole-cell currents were measured in fast and slow whole-cell patch-clamp experiments in cells grown either on filters or on coated plastic dishes. In addition the transepithelial voltage (V te) and resistance (R te) were measured in confluent monolayers. Resting cells had a membrane voltage (V m) of −36±1.1 mV (n=137) which was mainly caused by K+ and Cl− conductances and to a lesser extent by a Na+ conductance. V te was apical-side-negative after stimulation. Equivalent short-circuit current (I sc = V te/R te) was increased by the secretagogues histamine (0.1 mmol/l), bradykinin (0.1–10 μmol/l) and ATP (0.1–100 μmol/l). The histamine-induced I sc was blocked by either basolateral diphenhydramine (0.1 mmol/l, n=4) or apical cimetidine (0.1 mmol/l, n=4). In fast and slow whole-cell recordings ATP and bradykinin primarily activated a transient K+ conductance and hyperpolarized V m. This effect was mimicked by the Ca2+ ionophore ionomycin (1 μmol/l, n=11). Inhibition of the bradykinin-induced I sc by the blocker HOE140 (1 μmol/l, n=3) suggested the presence of a BK2 receptor. The potency sequence of different nucleotide agonists on the purinergic receptor was UTP ≈ ATP 〉 ITP 〉 GTP ≈ CTP ≈ [β,γ-methylene] ATP ≈ 2-methylthio-ATP = 0 and was obtained in I sc measurements and patch-clamp recordings. This suggests the presence of a P2u receptor. Hypotonic cell swelling activated both Cl− and K+ conductances. The Cl− conductance was only slightly inhibited by 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (0.5 mmol/ l, n=3). These data indicate that 16HBE140- bronchial epithelial cells, which are known to express high levels of cystic fibrosis transmembrane conductance regulator protein, form a secretory epithelium. While hypotonic cell swelling activates both K+ and Cl− channels, the Ca2+-induced Cl− secretion is due mainly to activation of basolateral K+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374583
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Effect of bradykinin and histamine on the membrane voltage, ion conductances and ion channels of human glomerular epithelial cells (hGEC) in culture (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 137-144 
    Details
    ISSN: 1432-2013
    Keywords: Human glomerular epithelial cells ; Bradykinin ; Histamine ; Nystatin patch clamp technique ; K+ conductance ; Maxi K+ channel ; Cl− conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of bradykinin (BK) and histamine (Hist) on the membrane voltage (V m), ion conductances and ion channels of cultured human glomerular epithelial cells (hGEC) were examined with the nystatin patch clamp technique. Cells were studied between passage 3 and 20 in a bath rinsed with Ringer-like solution at 37°C. The mean value of V m was −41±0.5 mV (n=189). BK (10−6 mol/l, n=29) and Hist (10−5 mol/l, n= 55) induced a rapid transient hyperpolarization by 15±1 mV and 18±1 mV, respectively. The hyperpolarization was followed by a long lasting depolarization by 6±1 mV (BK 10−6 mol/l) and 7±1 mV (Hist 10−5 mol/l). The ED50 was about 5×10−8 mol/l for BK and 5×10−7 mol/l for Hist. In the presence of both agonists, increases of outward and inward currents were observed. A change in the extracellular K+ concentration from 3.6 to 30 mmol/l depolarized V m by 8±1 mV and completely inhibited the hyperpolarizing effect of both agents (n=11). Reduction of extracellular Cl− concentration from 145 to 30 mmol/l led to a depolarization by 2 ±1 mV (n=25). In 30 mmol/l Cl− the depolarizations induced by BK (10−7 mol/l) and Hist (10−6 mol/l) were augmented to 9±2 mV (n=14) and to 10±2 mV (n=11), respectively. Ba2+ (5 mmol/l) depolarized V m by 19±5 mV (n=6) and completely inhibited the hyperpolarization induced by BK (10−6 mol/l, n=3) and reduced that of Hist (10−5 mol/l) markedly (n=3). Preincubation with the K+ channel blocker charybdotoxin (1–10 nmol/l) for 3 min had no significant effect on V m, but reduced markedly the BK(10−6 mol/l, n=11) and Hist-(10−5 mol/l, n=6) induced hyperpolarizations. In 10 out of 31 experiments in the cell attached nystatin patch configuration big K+ channels with a conductance $$(g_{K^ + } )$$ of 247±17 pS were found. The open probability of these K+ channels was increased 3- to 5-fold during the hyperpolarization induced by BK (10−7 mol/l) or Hist (10−5 mol/l, both n= 4). In excised inside/out patches this K+ channel had a mean conductance of 136±8.5 pS (n=10, clamp voltage 0 mV). The channel was outwardly rectifying and its open probability was increased when Ca2+ on the cytosolic side was greater than 0.1 μmol/l. The data indicate that BK and Hist activate a $$(g_{K^ + } )$$ and a $$g_{Cl^ - } $$ in hGEC. The hyperpolarization is induced by the activation of a Ca2+-dependent maxi K+ channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374604
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    A new class of inhibitors of cAMP-mediated Cl− secretion in rabbit colon, acting by the reduction of cAMP-activated K+ conductance (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 517-530 
    Details
    ISSN: 1432-2013
    Keywords: Cl− secretion ; Diarrhoea ; K+ conductance ; K+ channel blocker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previously we have shown that arylamino-benzoates like 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), which are very potent inhibitors of NaCl absorption in the thick ascending limb of the loop of Henle, are only poor inhibitors of the cAMP-mediated secretion of NaCl in rat colon. This has prompted our search for more potent inhibitors of NaCl secretion in the latter system. The chromanole compound 293 B inhibited the equivalent short-circuit current (I sc) induced by prostaglandin E2 (n=7), vasoactive intestinal polypeptide (VIP,n=5), adenosine (n=3), cholera toxin (n=4) and cAMP (n=6), but not by ionomycin (n=5) in distal rabbit colon half maximally (IC50) at 2 μmol/l from the mucosal and at 0.7 μmol/l from the serosal side. The inhibition was reversible and paralleled by a significant increase in transepithelial membrane resistance [e.g. in the VIP series from 116±16 Ω·cm2 to 136±21 Ω·cm2 (n=5)]. A total of 25 derivatives of 293 B were examined and structure activity relations were obtained. It was shown that the racemate 293 B was the most potent compound with-in this group and that its effect was due to the enantiomer 434 B which acted half maximally at 0.25 μmol/l. Further studies in isolated in vitro perfused colonic crypts revealed that 10 μmol/l 293 B had no effect on the membrane voltage across the basolateral membrane (V bl) in non-stimulated crypt cells: −69±3 mV versus −67±3 mV (n=10), whilst in the same cells 1 mmol/l Ba2+ depolarised (V bl) significantly. However, 293 B depolarised (V bl) significantly in the presence of 1 μmol/l forskolin: −45±4mV versus −39±5 mV (n=7). Similar results were obtained with 0.1 mmol/l adenosine. 293 B depolarised (V bl) from −40±5 mV to −30±4 mV (n=19). This was paralleled by an increase in the fractional resistance of the basolateral membrane. VIP had a comparable effect. The hyperpolarisation induced by 0.1 mmol ATP was not influenced by 10 μmol/l 293 B: −75±6 mV versus −75±6 mV (n=6). Also 293 B had no effect on basal K+ conductance (n=4). Hence, we conclude that 293 B inhibits the K+ conductance induced by cAMP. This conductance is apparently relevant for Cl− secretion and the basal K+ conductance is insufficient to support secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00704157
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    The effect of secretagogues on ion conductances of in vitro perfused, isolated rabbit colonic crypts (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 494-502 
    Details
    ISSN: 1432-2013
    Keywords: Cl− secretion ; cAMP ; K+ conductance ; Cl− conductance ; Diarrhoea
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Several secretagogues were used in this study, including those which enhance intracellular cyclic adenosine monophosphate (cAMP) production, as well as others which elevate intracellular Ca2+ activity and are known to increase Cl− secretion in the intact colon and in colonic carcinoma cell lines. They were examined with respect to their effects on electrophysiological properties in isolated rabbit distal colonic crypts. Crypts were dissected manually and perfused in vitro. Transepithelial voltage (V te), transepithelial resistance (R te), membrane voltage across the basolateral membrane (V bl), and fractional basolateral membrane resistance (FR bl), were estimated. Basolateral prostaglandin E2 (PGE2, ⩾0.1 μmol/l), vasoactive intestinal peptide (VIP, 1 nmol/l) and adenosine (0.1 mmol/l) induced an initial depolarisation and a secondary partial repolarisation of (V bl). In the case of adenosine, the initial depolarization of (V bl) was by 31±2 mV (n=47).R te fell significantly from 16.4±3.6 to 14.2±3.7 Ω·cm2 (n= 6), andFR blincreased significantly from 0.11±0.02 to 0.51±0.10 (n=6). In the second phase the repolarisation of (V bl) amounted 11±2 mV (n=47) and a steadystate (V bl) of −51±2 mV (n=47) was reached.R te fell further and significantly to a steady-state value of 12.4±3.8 Ω·cm2 (n=6) andFR bl fell significantly to 0.42±0.13 (n=6). In 30% of the experiments, a transient hyperpolarisation of (V bl) by 8±2 mV (n=14) was seen during wash out of adenosine. In the presence of adenosine, but not under control conditions, lowering of luminal Cl− concentration from 120 to 32 mmol/l depolarised (V bl) significantly by 8±1 mV (n=9). Basolateral ATP and ADP (0.1 mmol/l) led to a short initial depolarisation followed by a sustained and significant hyperpolarisation by 6±2 mV (n=27) and 5±4 mV (n=8), respectively. Carbachol (CCH) hyperpolarised (V bl) in a concentration-dependent manner. At 100 μmol/l (bath) the hyperpolarisation was by 14±2 mV (n=11) andFR bl fell slightly. Neurotensin (⩾10 nmol/l), isoproterenol (⩾10 μmol/l) and uridine 5′-triphosphate (UTP, 0.1 mmol/l) had no effect. It is concluded that PGE2, VIP and adenosine upregulate sequentially a luminal Cl− conductance and a basolateral K+ conductance by increasing intracellular cAMP concentration. Ca2+ mobilising hormones such as ATP, ADP, and CCH increase the basolateral K+ conductance, while the effect on luminal Cl− conductance appears to be very limited.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00704154
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Actin-dependent activation of ion conductances in bronchial epithelial cells (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 682-690 
    Details
    ISSN: 1432-2013
    Keywords: Cl− conductance ; K+ conductance ; Brefeldin A ; Cytochalasin D ; Epithelial cells ; Actin ; Microtubules
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Activation of Cl− and K+ channels is necessary to drive ion secretion in epithelia. There is substantial evidence from previous reports that vesicular transport and exocytosis are involved in the regulation of ion channels. In the present study we examined the role of cytoskeletal elements and components of intracellular vesicle transport on ion channel activation in bronchial epithelial cells. To this end, cells were incubated with a number of different compounds which interact with either microtubules or actin microfilaments, or which interfere with vesicle transport in the Golgi apparatus. The effectiveness of these agents was verified by fluorescence staining of cellular microtubules and actin. The function was examined in 36Cl− efflux studies as well as in whole-cell (WC) patch-clamp and cell-attached studies. The cells were studied under control conditions and after exposure to (in mmol/l) ATP (0.1), forskolin (0.01), histamine (0.01) and hypotonic bath solution (HBS, NaCl 72.5). In untreated control cells, ATP primarily activated a K+ conductance whilst histamine and forskolin induced mainly a Cl− conductance. HBS activated both K+ and Cl− conductances. Incubation of the cells with brefeldin A (up to 100 μmol/l) did not inhibit WC current activation and 36Cl− efflux. Nocodazole (up to 170 μmol/l) reduced the ATP-induced WC current, and mevastatin (up to 100 μmol/l) the cell-swelling-induced WC current. Neither had any effect on the WC current induced by forskolin and histamine. Also 36Cl− efflux induced by HBS, ATP, forskolin and histamine was unaltered by these compounds. Similarly, colchicine (10 μmol/l) and taxol (6 μmol/l) affected neither 36Cl− efflux nor WC current induced by ATP, forskolin, histamine or HBS. In contrast, depolymerisation of actin by cytochalasin D (10 μmol/l) significantly attenuated 36Cl− effluxes and WC current activation by the above-mentioned agonists. Incubation with a C2 clostridial toxin (5 nmol/l) showed similar effects on WC currents. Moreover, when cytochalasin D (10 μmol/l), C2 clostridial toxins (5 nmol/l), or phalloidin (10 μmol/l) were added to the pipette filling solution current activation was markedly reduced. However, in excised inside-out membrane patches, cytochalasin D (10 μmol/l), G-actin (10 μmol/l) and phalloidin (10 μmol/l) had no effect. These data suggest that actin participates in the activation of ion channels in 16HBE14o- epithelial cells and support the concept that exocytosis is a crucial step in the regulation of Cl− and K+ channels in these cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373989
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...