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  • Electronic Resource  (4)
  • Na+ channel kinetics  (2)
  • ADH  (1)
  • Bicarbonate permeability  (1)
  • 1
    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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    Paper (German National Licenses)
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  • 2
    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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  • 3
    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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  • 4
    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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