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  • 1
    Electronic Resource
    Electronic Resource
    Gating in iodate-modified single cardiac Na+ channels (1989)
    Springer
    The journal of membrane biology 112 (1989), S. 67-78 
    Details
    ISSN: 1432-1424
    Keywords: removal of Na+ inactivation ; iodate ; bromate ; glutaraldehyde ; DPI 201-106 ; Na+ channel kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Elementary Na+ currents were recorded at 19°C during 220-msec lasting step depolarizations in cell-attached and inside-out patches from cultured neonatal rat cardiocytes in order to study the modifying influence of iodate, bromate and glutaraldehyde on single cardiac Na+ channels. Iodate (10 mmol/liter) removed Na+ inactivation and caused repetitive, burst-like channel activity after treating the cytoplasmic channel surface. In contrast to normal Na+ channels under control conditions, iodate-modified Na+ channels attain two conducting states, a short-lasting one with a voltage-independent lifetime close to 1 msec and, likewise tested between −50 and +10 mV, a long-lasting one being apparently exponentially dependent on voltage. Channel modification by bromate (10 mmol/liter) and glutaraldehyde (0.5 mmol/liter) also included the occurrence of two open states. Also, burst duration depended apparently exponentially on voltage and increased when shifting the membrane in the positive direction, but there was no evidence for two bursting states. Chemically modified Na+ channels retain an apparently normal unitary conductance (12.8±0.5 pS). Of the two substates observed, one of them is remarkable in that it is mostly attained from full-state openings and is very short living in nature; the voltage-independent lifetime was close to 2 msec. Despite removal of inactivation, open probability progressively declined during membrane depolarization. The underlying deactivation process is strongly voltage sensitive but, in contrast to slow Na+ inactivation, responds to a voltage shift in the positive direction with a retardation in kinetics. Chemically modified Na+ channels exhibit a characteristic bursting state much shorter than in DPI-modified Na+ channels, a difference not consistent with the hypothesis of common kinetic properties in noninactivating Na+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871165
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  • 2
    Electronic Resource
    Electronic Resource
    Predominance of poorly reopening single Na+ channels and lack of slow Na+ inactivation in neonatal cardiocytes (1988)
    Springer
    The journal of membrane biology 103 (1988), S. 283-291 
    Details
    ISSN: 1432-1424
    Keywords: slow Na+ inactivation ; Na+ channel kinetics ; reopening ; neonatal cardiocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Elementary Na+ currents through single cardiac Na+ channels were recorded at −50 mV in cell-attached patches from neonatal rat cardiocytes kept at holding potentials between −100 and −120 mV. Na+ channel activity may occur as burst-like, closely-timed repetitive openings with shut times close to 0.5–0.6 msec, indicating that an individual Na+ channel may reopen several times during step depolarization. A systematic quantiative analysis in 19 cell-attached patches showed that reopening may be quite differently pronounced. The majority, namely 16 patches, contained Na+ channels with a low tendency to reopen. This was evidenced from the average value for the mean number of openings per sequence, 2.5. Strikingly different results were obtained in a second group of three patches. Here, a mean number of openings per sequence of 3.42, 3.72, and 5.68 was found. Ensemble averages from the latter group of patches revealed macroscopic Na+ currents with a biexponential decay phase. Reconstructed Na+ currents from patches with poorly reopening Na+ channels were devoid of a slow decay component. This strongly suggests that reopening may be causally related to slow Na+ inactivation. Poorly pronounced reopening and, consequently, the lack of slow Na+ inactivation could be characteristic features of neonatal cardiac Na+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01993988
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  • 3
    Electronic Resource
    Electronic Resource
    Single nonselective cation channels and Ca2+-activated K+ channels in aortic endothelial cells (1987)
    Springer
    The journal of membrane biology 98 (1987), S. 125-133 
    Details
    ISSN: 1432-1424
    Keywords: patch clamp ; ionic channels ; vascular endothelium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary In cultured bovine aortic endothelial cells, elementary K+ currents were studied in cell-attached and inside-out patches using the standard patch-clamp technique. Two different cationic channels were found, a large channel with a mean unitary conductance of 150±10 pS and a small channel with a mean unitary conductance of 12.5±1.1 pS. The 150-pS channel proved to be voltag- and Ca2+-activatable and seems to be a K+ channel. Its open probability increased on membrane depolarization and, at a given membrane potential, was greatly enhanced by elevating the Ca2+ concentration at the cytoplasmic side of the membrane from 10−7 to 10−4 m. 150-pS channels were not influenced by the patch configuration in that patch excision neither induced rundown nor evoked channel activity in silent cell-attached patches. However, they were only seen in two out of 55 patches. The 12-pS channel was predominant, a nonselective cationic channel with almost the same permeability for K+ and Na+ whose open probability was minimal near −60 mV but increased on membrane hyperpolarization. An increase in internal Ca2+ from 10−7 to 10−4 m left the open probability unchanged. Although the K+ selectivity of the 150-pS channels remains to be elucidated, it is concluded that they may be involved in controlling Ca2+-dependent cellular functions. Under physiological conditions, 12-pS nonselective channels may provide an inward cationic pathway for Na+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01872125
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  • 4
    Electronic Resource
    Electronic Resource
    Modification of single cardiac Na+ channels by DPI 201-106 (1986)
    Springer
    The journal of membrane biology 89 (1986), S. 163-172 
    Details
    ISSN: 1432-1424
    Keywords: inside-out patch clamp ; kinetic behavior of cardiac Na+ channels ; chemically eliminated inactivation ; piperazine indole ; isolated heart cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary In inside-out patches from cultured neonatal rat heart cells, single Na+ channel currents were analyzed under the influence of the cardiotonic compound DPI 201-106 (DPI), a putative novel channel modifier. In absence of DPI, normal cardiac single Na+ channels studied at −30 mV have one open state which is rapidly left with a rate constant of 826.5 sec−1 at 20°C during sustained depolarization., Reconstructed macroscopic currents relax completely with 7 to 10 msec. The current decay fits a single exponential. A considerable percentage of openings may occur during relaxation of the macroscopic current. In patches treated with 3×10−6 m DPI in the pipette solution, stepping to −30 mV results in drastically prolonged and usually repetitive openings. This channel activity mostly persists over the whole depolarization (usually 160 msec in duration) but is abruptly terminated on clamping back the patch to the holding potential. Besides these modified events, apparently normal openings occur. The open time distribution of DPI-treated Na+ channels is the sum of two exponentials characterized by time constants of 0.85 msec (which is close to the time constant found in the control patches, 1.21 msec) and 12 msec. Moreover, DPI-modified Na+ channels exhibit a sustained high, time-independent open probability. Similar to normal Na+ channels, the mean number of open DPI-modified Na+ channels is voltage-dependent and increases on shifting the holding potential in the hyperpolarizing direction. These kinetic changes suggest an elimination of Na+ channel inactivation as it may follow from an interaction of DPI with Na+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869712
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  • 5
    Electronic Resource
    Electronic Resource
    Removal of inactivation and blockade of cardiac Na+ channels by DPI 201-106 different voltage-dependencies of the drug actions (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 183-188 
    Details
    ISSN: 1432-1912
    Keywords: Non-decaying I Na ; IN, blockade ; Class III antiarrhythmic agents
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of the novel cardiotonic diphenylpiperazinylindole derivative. the racemic DPI 201-106. on cardiac Na+ channels was studied in conventional microelectrode experiments on papillary muscles of guinea pigs and in patch clamp experiments using inside-out patches excised from cultured neonatal rat cardiocytes. The maximal rate of rise (V max) of Na+-dependent action potentials was taken as an estimate for INa. Racemic DPI (3 × 10−6 mol/1) exerts a dual effect as it removes channel inactivation and may also block cardiac Na+ channels. Both drug actions proved highly voltage-dependent but a given change in membrane potential had a strictly different modulating influence on the two effects. The \0V max depression induced by racemic DPI became attenuated due to hyperpolarization and finally tended to disappear at about -90 mV. while at the same time I Na modification became increasingly accentuated. An increase in holding potential caused the non-decaying portion of the macroscopic I Na to increase significantly. Resting inactivation remained operative in non-inactivating cardiac Na+ channels and showed a similar voltage-dependence as in normal Na+ channels. The differential voltage-dependencies of both DPI effects strongly suggest the existence of two binding sites for DPI.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00177721
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  • 6
    Electronic Resource
    Electronic Resource
    Single cardiac outwardly rectifying K+ channels modulated by protein kinase A and a G-protein (1991)
    Springer
    European biophysics journal 20 (1991), S. 281-286 
    Details
    ISSN: 1432-1017
    Keywords: Cardiac K+ channels ; Phosphorylation ; GTP ; GDP ; Neonatal rat heart myocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Physics
    Notes: Abstract Elementary K+ currents were recorded at 19 °C in cell-attached and in inside-out patches excised from neonatal rat heart myocytes. An outwardly rectifying K+ channel which prevented Na+ ions from permeating could be detected in about 10% of the patches attaining (at 5 mmol/l external K+ and between − 20 mV and + 20 mV) a unitary conductance of 66 +- 3.9 pS. K (outw.-rect.) + channels have one open and at least two closed states. Open probability and τopen rose steeply on shifting the membrane potential in the positive direction, thereby tending to saturate. Open probability (at −7 mV) was as low as 3 ± 1% but increased several-fold on exposing the cytoplasmic surface to Mg-ATP (100 μmol/l) without a concomitant change of τopen. No channel activation occurred in response to ATP in the absence of cytoplasmic Mg−+. The cytoplasmic administration of the catalytic subunit of protein kinase A (120–150 μ/ml) or GTP-γ-S (100 μmol/l) caused a similar channel activation. GDP-β-S (100 μmol/l) was also tested and found to be ineffective in this respect. This suggests that cardiac K (outw.-rect.) + channels are metabolically modulated by both cAMP-dependent phosphorylation and a G-protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00450563
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  • 7
    Electronic Resource
    Electronic Resource
    Differences in open state of NBA-modified cardiac Na+ channels (1988)
    Springer
    European biophysics journal 15 (1988), S. 289-292 
    Details
    ISSN: 1432-1017
    Keywords: Patch clamp ; cardiac Na+ channels ; channel modification ; heterogeneous population
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Physics
    Notes: Abstract Patch clamp recordings from neonatal cardiac Na+ channels treated with N-bromoacetamide (NBA, 5–50 x 10-mol/l) showed modified Na+ channel activity. By chemical removal of inactivation, repetitive openings with an increased life time and burst-like activity occurred. NBA-modified Na+ channels differ in life time and may attain either a slightly (mean open time 3.1±0.2 ms) or a strongly (mean open time 15.2±1.4 ms) prolonged open state. This strongly suggests a heterogeneous population of NBA-modified Na+ channels in newborn rat cardiocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00256479
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  • 8
    Electronic Resource
    Electronic Resource
    Cation specificity and pharmacological properties of the Ca2+-dependent K+ channel of rat cortical collecting ducts (1993)
    Springer
    Pflügers Archiv 422 (1993), S. 481-491 
    Details
    ISSN: 1432-2013
    Keywords: Patch clamp ; Verapamil ; Charyb-dotoxin ; Apamin ; K+ channel blocker ; Permselectivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The luminal membrane of principal cells of rat cortical collecting duct (CCD) is dominated by a K+ conductance. Two different K+ channels are described for this membrane. K+ secretion probably occurs via a small-conductance Ca2+-independent channel. The function of the second, large-conductance Ca2+-dependent channel is unclear. This study examines properties of this channel to allow a comparison of this K+ channel with the macroscopic K+ conductance of the CCD and with similar K+ channels from other preparations. The channel is poorly active on the cell. It has a conductance of 263±11 pS (n=36, symmetrical K+ concentrations) and of 139±3 pS (n=91) with 145 mmol/l K+ on one side and 3.6 mmol/l K+ on the other side of the membrane. Its open probability is high after excision (0.71±0.03, n=85). The channel flickers rapidly between open and closed states. Its permeability in the cell-free configuration was 7.0±0.2×10−13 cm3/s (n=85). It is inhibited by several typical blockers of K+ channels such as Ba2+, tetraethylammonium, quinine, and quinidine and high concentrations of Mg2+. The Ca2+ antagonists verapamil and diltiazem also inhibit this K+ channel. As is typical for the maxi K+ channel, it is inhibited by charybdotoxin but not by apamin. The selectivity of this large-conductance K+ channel demonstrates significant differences between the permeability sequence (P K 〉 P Rb 〉 P NH4 〉 P Cs=P Li=P Na=P choline=0) and the conductance sequence (g K 〉 g NH4 〉 g Rb 〉 g Li=g choline 〉 g Cs=g Na=0). The only other cations that are significantly conducted by this channel besides K+ (g K at V c =∞ is 279±8 pS, n=88) are NH 4 + (g NH4=127±22 pS, n=10) and Rb+ (g Rb=36±5 pS, n=6). The K+ currents through this channel are reduced by high concentrations of choline+, Cs+, Rb+, and NH 4 + . These properties and the dependence of this channel on Ca2+ and voltage classify it as a “maxi” K+ channel. A possible physiological function of this channel is discussed in the accompanying paper.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00375076
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  • 9
    Electronic Resource
    Electronic Resource
    Bicarbonate permeability of epithelial chloride channels (1991)
    Springer
    Pflügers Archiv 417 (1991), S. 616-621 
    Details
    ISSN: 1432-2013
    Keywords: Bicarbonate permeability ; Bicarbonate conductance ; Cl− channels ; HT29 ; T84 ; Respiratory cells ; Bicarbonate channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bicarbonate permeability of epithelial chloride channels has been studied using the patch-clamp technique. The experiments were performed in excised insideout oriented membrane patches from three different cultured cell types: (a) HT29 colon carcinoma cell line, (b) T84 colon carcinoma cell line, and (c) respiratory epithelial cells (REC) in primary culture. In all three preparations we observed outwardly rectifying chloride channels with similar conductances with 145 mmol/l NaCl solution in the pipette and in the bath (Cl− pipette/ Cl− bath). When Cl− was replaced by HCO 3 − in the bath (Cl−/HCO 3 − ) the conductance of the channel at negative clamp voltages was reduced significantly by 40% for HT29 (n=6), 39% for T84 (n=7), and 38% for REC (n=6). Similarly, the zero-current potential (VI=0) was shifted from 0 mV (Cl−/Cl−) to negative values (Cl−/ HCO 3 − ) revealing permeability ratios $${{P_{{\text{Cl}}} } \mathord{\left/ {\vphantom {{P_{{\text{Cl}}} } {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}} \right. \kern-\nulldelimiterspace} {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}$$ of 2.4±0.1 for HT29 (n=6), 2.0±0.1 for T84 (n=7), and 1.8±0.1 for REC (n=7). With NaHCO3 as the pipette solution and NaCl in the bath, the VI=0 was positive and a $${{P_{{\text{Cl}}} } \mathord{\left/ {\vphantom {{P_{{\text{Cl}}} } {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}} \right. \kern-\nulldelimiterspace} {P_{{\text{H}}_{{\text{CO}}_{\text{3}} } } }}$$ , value of 2.3±0.1 was determined for HT29 (n=5). Replacement of Cl− in the bath by HCO 3 − reduced V I=0 to values close to 0 mV. In another series of experiments, the pipette was filled with 145 mmol/l NaCl and the bath contained 35 mmol/l NaCl to which 35 mmol/l NaHCO3 were added. We found that neither the conductance for the inward current nor VI=0 was changed significantly with the additon of NaHCO3 (HT29, n=6). We conclude that the HCO 3 − permeability and HCO 3 − conductance of these channels is about half of that for Cl−.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00372960
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  • 10
    Electronic Resource
    Electronic Resource
    Antidiuretic hormone acts via V1 receptors on intracellular calcium in the isolated perfused rabbit cortical thick ascending limb (1991)
    Springer
    Pflügers Archiv 417 (1991), S. 622-632 
    Details
    ISSN: 1432-2013
    Keywords: ADH ; V1 receptor ; dDAVP ; Intracellular Ca2+ ; Fura-2 ; In vitro microperfusion ; Rabbit kidney ; Cortical thick ascending limb
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of antidiuretic hormone ([Arg]vasopressin, ADH) on intracellular calcium activity [Ca2+]i of isolated perfused rabbit cortical thick ascending limb (cTAL) segments was investigated with the calcium fluorescent dye fura-2. The fluorescence emission ratio at 500–530 nm (R) was monitored as a measure of [Ca2+]i after excitation at 335 nm and 380 nm. In addition the transepithelial potential difference (PD te) and transepithelial resistance (R te) of the tubule were measured simultaneously. After addition of ADH (1–4 nmol/l) to the basolateral side of the cTAL R increased rapidly, but transiently, from 0.84±0.05 to 1.36±0.08 (n = 46). Subsequently, within 7–12 min R fell to control values even in the continued presence of ADH. The increase in R evoked by the ADH application corresponded to a rise of [Ca2+]i from a basal level of 155±23 nmol/l [Ca2+]i up to 429±53 nmol/l [Ca2+]i at the peak of the transient, as estimated by intra- or extracellular calibration procedures. The electrical parameters (PD te and R te) of the tubules were not changed by ADH. The ADH-induced Ca2+ transient was dependent on the presence of Ca2+ on the basolateral side, whereas luminal Ca2+ had no effect. d(CH2)5[Tyr(Me)2]2,Arg8vasopressin, a V1 antagonist (Manning compound, 10 nmol/l), blocked the ADH effect on [Ca2+]i completely (n = 5). The V2 agonist 1-desamino-[d-Arg8]vasopressin (10 nmol/l, n=4), and the cAMP analogues, dibutyryl-cAMP (400 μmol/l, n = 4), 8-(4-chlorophenylthio)-cAMP (100 μmol/l, n = 1) or 8-bromo-cAMP (200 μmol/1, n = 4) had no influence on [Ca2+]i. The ADH-induced [Ca2+]i increase was not sensitive to the calcium-channel blockers nifedipine and verapamil (100 μmol/l, n = 4). We conclude that ADH acts via V1 receptors to increase cytosolic calcium activity transiently in rabbit cortical thick ascending limb segments, possibly by an initial Ca2+ release from intracellular stores and by further Ca2+ influx through Ca2+ channels in the basolateral membrane. These channels are insensitive to L-type Ca2+ channel blockers, e.g. nifedipine and verapamil.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00372961
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