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  • 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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  • 2
    Electronic Resource
    Electronic Resource
    Agonist-induced intracellular Ca2+ transients in HT29 cells (1993)
    Springer
    Pflügers Archiv 423 (1993), S. 519-526 
    Details
    ISSN: 1432-2013
    Keywords: Carbachol ; Adenosine triphosphate ; Neurotensin ; Fura-2 ; Intracellular Ca2+ ; Ca2+ influx ; Mn2+ ; Verapamil ; Ni2+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the present study we have investigated the mechanism of intracellular Ca2+ activity ([Ca2+]i) changes in HT29 cells induced by adenosine triphosphate (ATP), carbachol (CCH), and neurotensin (NT). [Ca2+]i was measured with the fluorescent Ca2+ indicator fura-2 at the single-cell level or in small cell plaques with high time resolution (1–40Hz). ATP and CCH induced not only a dose-dependent [Ca2+]i peak response, but also changes of the plateau phase. The [Ca2+]i plateau was inversely dependent on the ATP concentration, whereas the CCH-induced [Ca2+]i plateau increased at higher CCH concentrations. NT showed (from 10−10 to 10−7 mol/l) in most cases only a [Ca2+]i spike lasting 2–3 min. The [Ca2+]i plateau induced by ATP (10−6 mol/l) and CCH (10−5 mol/l) was abolished by reducing the Ca2+ activity in the bath from 10−3 to 10−4 mol/l (n=7). In Ca2+-free bathing solution the [Ca2+]i peak value for all three agonists was not altered. Using fura-2 quenching by Mn2+ as an indicator of Ca2+ influx the [Ca2+]i peak was always reached before Mn2+ influx started. Every agonist showed this delayed stimulation of the Ca2+ influx with a lag time of 23±1.5 s (n=15) indicating a similar mechanism in each case. Verapamil (10−6–10−4 mol/l) blocked dose dependently both phases (peak and plateau) of the CCH-induced [Ca2+]i increase. Short pre-incubation with verapamil augmented the effect on the [Ca2+]i peak, whereas no further influence on the plateau was observed. Ni2+ (10−3 mol/l) reduced the plateau value by 70%.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374950
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  • 3
    Electronic Resource
    Electronic Resource
    Evidence for agonist-induced export of intracellular Ca2+ in epithelial cells (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 423-430 
    Details
    ISSN: 1432-2013
    Keywords: [Ca2+]i export ; Thapsigargin ; fura-2 ; HT29 ; CFPAC-1 ; ATP ; Carbachol ; Neurotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is increasing evidence that some agonists not only induce intracellular Ca2+ increases, due to store release and transmembranous influx, but also that they stimulate Ca2+ efflux. We have investigated the agonist-stimulated response on the intracellular Ca2+ activity ([Ca2+]i) in the presence of thapsigargin (10−8 mol/l, TG) in HT29 and CFPAC-1 cells. For CFPAC-1 the agonists ATP (10−7–10−3 mol/l, n=9), carbachol (10−6–10−3 mol/l, n=5) and neurotensin (10−10–10−7 mol/l, n=6) all induced a concentration-dependent decrease in [Ca2+]i in the presence of TG. Similar results were obtained with HT29 cells. This decrease of [Ca2+]i could be caused by a reduced Ca2+ influx, either due to a reduced driving force for Ca2+ in the presence of depolarizing agonists or due to agonist-regulated decrease in Ca2+ permeability. Using the fura-2 Mn2+ quenching technique we demonstrated that ATP did not slow the TG-induced Mn2+ quench. This indicates that the agonist-induced [Ca2+]i decrease in the presence of TG was not due to a reduced influx of Ca2+ into the cell, but rather due to stimulation of Ca2+ export. We used the cell attached nystatin patch clamp technique in CFPAC-1 cells to examine whether, in the presence of TG, the above agonists still led to the previously described electrical changes. The cells had a mean membrane voltage of −49±3.6 mV (n=9). Within the first 3 min ATP was still able to induce a depolarization which could be attributed to an increase in Cl− conductance. This was expected, since at this time after TG stimulation all Ca2+ agonists still liberated some [Ca2+]i. When TG incubation was prolonged, agonist application led to strongly attenuated or to no electrical responses. Therefore, the agonist-stimulated [Ca2+]i decrease cannot be explained by the reduction of the driving force for Ca2+ into the cell. In the same cells hypotonic swelling (160 mosmol/l, n=15) still induced a further [Ca2+]i increase in the presence of TG and concomitantly induced Cl− and K+ conductances. We conclude that the agonist-induced decrease of [Ca2+]i in the presence of TG probably unmasks a stimulation of [Ca2+]i export.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374904
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