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  • 1
    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.
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  • 2
    ISSN: 1432-2013
    Keywords: Parathyroid hormone ; Human calcitonin ; Transepithelial ion net fluxes ; Na+, Cl−, K+, Mg2+, Ca2+ transport ; Electron microprobe analysis-Mouse kidney ; In vitro microperfusion ; Cortical and medullary thick ascending limb of Henle's loop
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of parathyroid hormone (PTH) on transepithelial Na+, Cl−, K+, Ca2+ and Mg2+ transport was investigated in isolated perfused cortical thick ascending limbs (cTAL) and that of human calcitonin (hCT) was tested in both cortical and medullary thick ascending limbs (mTAL) of the mouse nephron. The transepithelial ion net fluxes (J x) were determined by electron probe analysis of the perfused and collected fluids. Simultaneously, the transepithelial voltage (PDte) and resistance (R te) were recorded. In cTAL segments, PTH and hCT significantly stimulated the reabsorption of Na+, Cl−, Ca2+ and Mg2+. hCT generated a net K+ secretion towards the lumen and PTH tended to exert the same effect. Neither PDte nor R te were significantly altered by either PTH or hCT. However, in the post-experimental period a significant decrease in PDte was noted. Time control experiments carried out under similar conditions revealed a significant decrease in PDte with time, which could have masked the hormonal response. In mTAL segments, Mg2+ and Ca2+ transport was close to zero. hCT did not exert any detectable effect on either PDte or J Cl −, J Na + J K +, J Mg 2+ and J Ca 2+ in these segments. In conclusion, our data demonstrate that PTH and hCT stimulate NaCl reabsorption as well as Mg2+ and Ca2+ reabsorption in the cTAL segment of the mouse. These data are in agreement with and extend data obtained in vivo in the rat.
    Type of Medium: Electronic Resource
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  • 3
    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
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 419 (1991), S. 472-477 
    ISSN: 1432-2013
    Keywords: Glucagon ; Transepithelial ion net fluxes ; Water, Na+, Cl−, K+, Mg2+, Ca2+, transport ; Electron microprobe ; Rat kidney ; In vivo micropuncture study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of glucagon on water and electrolyte transport in the kidney were investigated on hormone-deprived rats, i.e. thyroparathyroidectomized diabetes insipidus Brattleboro rats infused with somatostatin. Glucagon consistently inhibited the reabsorption of water and Na+, Cl−, K+ and Ca2+ along the proximal tubule accessible to micropuncture, leaving the reabsorption of inorganic phosphate (Pi) untouched. In the loop, besides its previously described stimulatory effects on Na+, Cl−, K+, Ca2+ and Mg2+ reabsorption, glucagon strongly inhibited Pi reabsorption, very probably in the proximal straight tubule. These effects resulted in a significant phosphaturia and considerable reductions of Mg2+ and Ca2+ excretions. The effects of glucagon at both the whole kidney and the nephron levels are very similar to those previously described for calcitonin. In the absence of an adenylate cyclase system sensitive to glucagon and calcitonin in the rat proximal tubule, and from the analogy of their physiological effects with those elicited by parathyroid hormone, it is suggested that glucagon and calcitonin exert their inhibitory effects on Na and Pi reabsorption in the proximal tubule through another pathway, which could be the phosphoinositide regulatory cascade.
    Type of Medium: Electronic Resource
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