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
  • Electronic Resource  (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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 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
    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...