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  • ADH  (2)
  • Ca2+ influx  (2)
  • Electron microprobe  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Differential effects of ADH on sodium, chloride, potassium, calcium and magnesium transport in cortical and medullary thick ascending limbs of mouse nephron (1988)
    Springer
    Pflügers Archiv 412 (1988), S. 516-523 
    Details
    ISSN: 1432-2013
    Keywords: ADH ; Transepithelial ion net fluxes ; Na+, Cl−, K+, Ca2+ and Mg2+ transport ; Electron microprobe ; Mouse kidney ; Cortical and medullary thick ascending limb of Henle's loop ; In vitro microperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of antidiuretic hormone (arginine vasopressin, AVP) on transepithelial Na+, Cl−, K+, Ca2+ and Mg2+ net transports was investigated in medullary (mTAL) and cortical (cTAL) segments of the thick ascending limb (TAL) of mouse nephron, perfused in vitro. Transepithelial net fluxes (J Na +,J Cl −,J K +,J Ca 2+,J Mg 2+) were determined by electron probe analysis of the collected tubular fluid. Transepithelial potential difference (PDte) and transepithelial resistance (Rte) were measured simultaneously. cTAL segments were bathed and perfused with isoosmolal, HCO 3 − containing Ringer solutions, mTAL segments were bathed and perfused with isoosmolal HCO 3 − free Ringer solutions. In cTAL segments, AVP (10−10 mol·l−1) significantly increasedJ Mg 2+ andJ Ca 2+ from 0.39±0.08 to 0.58±0.10 and from 0.86±0.13 to 1.19±0.15 pmol·min−1 mm−1 respectively. NeitherJ Na + norJ Cl −, (J Na +: 213±30 versus 221±28 pmol·min−1 mm−1,J Cl −: 206±30 versus 220±23 pmol·min−1 mm−1) nor PDte (13.4±1.3 mV versus 14.1±1.9 mV) or Rte (24.6±6.5Ω cm2 versus 22.6±6.4Ω cm2) were significantly changed by AVP. No significant effect of AVP on net K+ transport was observed. In mTAL segments, Mg2+ and Ca2+ net transports were close to zero and AVP (10−10 mol·l−1) elicited no effect. However NaCl net reabsorption was significantly stimulated by the hormone,J Na + increased from 107±33 to 148±30 andJ Cl − from 121±33 to 165±32 pmol·min−1 mm−1. The rise inJ NaCl was accompanied by an increase in PDte from 9.0±0.7 to 13.5±0.9 mV and a decrease in Rte from 14.4±2.0 to 11.2±1.7 Ω cm2. No K+ net transport was detected, either under control conditions or in the presence of AVP. To test for a possible effect of HCO 3 − on transepithelial ion fluxes, mTAL segments were bathed and perfused with HCO 3 − containing Ringer solutions. With the exception ofJ Ca 2+ which was significantly different from zero (J Ca 2+: 0.26±0.06 pmol·min−1 mm−1), net transepithelial fluxes of Na+, Cl−, K+ and Mg2+ were unaffected by HCO 3 − . In the presence of AVP,J Mg 2+ andJ Ca 2+ were unaltered whereasJ NaCl was stimulated to the same extent as observed in the absence of HCO 3 − . In conclusion our results indicate heterogeneity of response to AVP in cortical and medullary segments of the TAL segment, since AVP stimulates Ca2+ and Mg2+ reabsorption in the cortical part and Na+ and Cl− reabsorption in the medullary part of this nephron segment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00582541
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of glucagon on Na+, Cl−, K+, Mg2+ and Ca2+ transports in cortical and medullary thick ascending limbs of mouse kidney (1989)
    Springer
    Pflügers Archiv 414 (1989), S. 640-646 
    Details
    ISSN: 1432-2013
    Keywords: Glucagon ; Transepithelial ion net fluxes ; Na+, Cl−, K+, Ca2+, Mg2+ transport ; Electron microprobe ; Mouse kidney ; In vitro microperfusion ; Cortical and medullary thick ascending limb of Henle's loop ; In vivo micropuncture study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of glucagon on transepithelial Na+, Cl−, K+, Ca2+ and Mg2+ net fluxes were investigated in isolated perfused cortical (cTAL) and medullary (mTAL) thick ascending limbs of Henle's loop of the mouse nephron. Transepithelial ion net fluxes (J Na +,J Cl −,J K +,J Ca 2+,J Mg 2+) were determined by electron probe analysis of the collected tubular fluid. Simultaneously the transepithelial voltage (PDte) and the transepithelial resistance (R te) were recorded. In cTAL-segments (n=8), glucagon (1.2×10−8 mol · l−1) stimulated significantly the reabsorption of Na+, Cl−, Ca2+ and Mg2+∶J Na + increased from 204±20 to 228±23 pmol · min−1 · mm−1,J Cl − from 203±18 to 234±21 pmol · min−1 · mm−1,J Ca 2+ from 0.52±0.13 to 1.34±0.30 pmol · min−1 · mm−1 andJ Mg 2+ from 0.51±0.08 to 0.84±0.08 pmol · min−1 · mm−1.J K+ remained unchanged: 3.2±1.3 versus 4.0±1.9 pmol · min−1 · mm−1. Neither PDte (16.3±1.5 versus 15.9±1.4 mV) norR te (22.5±3.0 versus 20.3±2.6 Ωcm2) were changed significantly by glucagon. However, in the post-experimental periods a significant decrease in PDte and increase inR te were noted. In mTAL-segments (n=9), Mg2+ and Ca2+ transports were close to zero and glucagon elicited no significant effect. The reabsorptions of Na+ and Cl−, however, were strongly stimulated:J Na + increased from 153±17 to 226±30 pmol · min−1 · mm−1 andJ Cl − from 151±23 to 243±30 pmol · min−1 · mm−1. The rise in NaCl transport was accompanied by an increase in PDte from 10.3±1.1 to 12.3±1.2 mV and a decrease inR te from 19.1±2.7 to 17.8±2.0 Ωcm2. No net K+ movement was detectable either in the absence or in the presence of glucagon. A micropuncture study carried out in hormone-deprived rats indicated that glucagon stimulates Na+, Cl−, K+, Mg2+ and Ca2+ reabsorptions in the loop of Henle. In conclusion our data demonstrate that glucagon stimulates NaCl reabsorption in the mTAL segment and to a lesser extent in the cTAL segment whereas it stimulates Ca2+ and Mg2+ reabsorptions only in the cortical part of the thick ascending limb of the mouse nephron. These data are in good agreement with, and extend, those obtained in vivo on the rat with the hormone-deprived model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00582129
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  • 3
    Electronic Resource
    Electronic Resource
    The effect of intracellular pH on cytosolic Ca2+ in HT29 cells (1996)
    Springer
    Pflügers Archiv 433 (1996), S. 98-108 
    Details
    ISSN: 1432-2013
    Keywords: Key words CO2/HCO3 ; NH3/NH4+ ; pHi ; [Ca2+]i ; Fura-2 ; BCECF ; Ca2+ store ; Ca2+ influx ; Inositol 1 ; 4 ; 5-trisphosphate ; Epithelia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The influence of intracellular pH (pHi) on intracellular Ca2+ activity ([Ca2+]i) in HT29 cells was examined microspectrofluorometrically. pHi was changed by replacing phosphate buffer by the diffusible buffers CO2/HCO3 –or NH3/NH4 + (pH 7.4). CO2/HCO3 –buffers at 2,5 or 10% acidified pHi by 0.1, 0.32 and 0.38 pH units, respectively, and increased [Ca2+]i by 8–15 nmol/l. This effect was independent of the extracellular Ca2+ activity and the filling state of thapsigargin-sensitive Ca2+ stores. Removing the CO2/HCO3 –buffer alkalinized pHi by 0.14 (2%), 0.27 (5%), and 0.38 (10%) units and enhanced [Ca2+]i to a peak value of 20, 65, and 143 nmol/l, respectively. Experiments carried out with Ca2+-free solution and with thapsigargin showed that the [Ca2+]i transient was due to release from intracellular pools and stimulated Ca2+ entry. NH3/NH4 + (20 mmol/l) induced a transient intracellular alkalinization by 0.6 pHunits and increased [Ca2+]i to a peak (Δ [Ca2+]i = 164 nmol/l). The peak [Ca2+]i increase was not influenced by removal of external Ca2+, but the decline to basal [Ca2+]i was faster. Neither the phospholipase C inhibitor U73122 nor the inositol 1,4,5-trisphosphate (InsP 3) antagonist theophylline had any influence on the NH3/NH4 +-stimulated [Ca2+]i increase, whereas carbachol-induced [Ca2+]i transients were reduced by more than 80% and 30%, respectively. InsP 3 measurements showed no change of InsP 3 during exposure to NH3/NH4 +, whereas carbachol enhanced the InsP 3 concentration, and this effect was abolished by U73122. The pHi influence on ”capacitative” Ca2+ influx was also examined. An acid pHi attenuated, and an alkaline pHi enhanced, carbachol- and thapsigargin-induced [Ca2+]i influx. We conclude that: (1) an alkaline pHi releases Ca2+ from InsP 3-dependent intracellular stores; (2) the store release is InsP 3 independent and occurs via an as yet unknown mechanism; (3) the store release stimulates capacitative Ca2+ influx; (4) the capacitative Ca2+ influx activated by InsP 3 agonists is decreased by acidic and enhanced by alkaline pHi. The effects of pHi on [Ca2+]i should be of relevance under many physiological conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050254
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  • 4
    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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  • 5
    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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