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  • 1
    ISSN: 1432-1424
    Keywords: Key words: Cl− Channel — Organic Anions — Phosphate — NPPB
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. Expression of the protein NaPi-1 in Xenopus oocytes has previously been shown to induce an outwardly rectifying Cl− conductance (GCl), organic anion transport and Na+-dependent P i -uptake. In the present study we investigated the relation between the NaPi-1 induced GCl and P i -induced currents and transport. NaPi-1 expression induced P i -transport, which was not different at 1–20 ng/oocyte NaPi-1 cRNA injection and was already maximal at 1–2 days after cRNA injection. In contrast, GCl was augmented at increased amounts of cRNA injection (1–20 ng/oocyte) and over a five day expression period. Subsequently all experiments were performed on oocytes injected with 20 ng/oocytes cRNA. P i -induced currents (Ip) could be observed in NaPi-1 expressing oocytes at high concentrations of P i (≥ 1 mm P i ). The amplitudes of Ip correlated well with GCl. Ip was blocked by the Cl− channel blocker NPPB, partially Na+-dependent and completely abolished in Cl− free solution. In contrast, P i -transport in NaPi-1 expressing oocytes was not NPPB sensitive, stronger depending on extracellular Na+ and weakly affected by Cl− substitution. Endogenous P i -uptake in water-injected oocytes amounted in all experiments to 30–50% of the Na+-dependent P i -transport observed in NaPi-1 expressing oocytes. The properties of the endogenous P i -uptake system (K m for P i 〉 1 mm; partial Na+- and Cl−-dependence; lack of NPPB block) were similar to the NaPi-1 induced P i -uptake, but no Ip could be recorded at P i -concentrations ≤3 mm. In summary, the present data suggest that Ip does not reflect charge transfer related to P i -uptake, but a P i -mediated modulation of GCl.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1424
    Keywords: Key words: Na+/Pi cotransporter — Proximal tubule — Voltage clamp — Steady-state — Presteady-state —Xenopus laevis oocyte expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract: The two electrode voltage clamp technique was used to investigate the steady-state and presteady-state kinetic properties of the type II Na+/P i cotransporter NaPi-5, cloned from the kidney of winter flounder (Pseudopleuronectes americanus) and expressed in Xenopus laevis oocytes. Steady-state P i -induced currents had a voltage-independent apparent K m for P i of 0.03 mm and a Hill coefficient of 1.0 at neutral pH, when superfusing with 96 mm Na+. The apparent K m for Na+ at 1 mm P i was strongly voltage dependent (increasing from 32 mm at −70 mV to 77 mm at −30 mV) and the Hill coefficient was between 1 and 2, indicating cooperative binding of more than one Na+ ion. The maximum steady-state current was pH dependent, diminishing by 50% or more for a change from pH 7.8 to pH 6.3. Voltage jumps elicited presteady-state relaxations in the presence of 96 mm Na+ which were suppressed at saturating P i (1 mm). Relaxations were absent in non-injected oocytes. Charge was balanced for equal positive and negative steps, saturated at extremes of potential and reversed at the holding potential. Fitting the charge transfer to a Boltzmann relationship typically gave a midpoint voltage (V 0.5) close to zero and an apparent valency of approximately 0.6. The maximum steady-state transport rate correlated linearly with the maximum P i -suppressed charge movement, indicating that the relaxations were NaPi-5-specific. The apparent transporter turnover was estimated as 35 sec−1. The voltage dependence of the relaxations was P i -independent, whereas changes in Na+ shifted V 0.5 to −60 mV at 25 mm Na+. Protons suppressed relaxations but contributed to no detectable charge movement in zero external Na+. The voltage dependent presteady-state behavior of NaPi-5 could be described by a 3 state model in which the partial reactions involving reorientation of the unloaded carrier and binding of Na+ contribute to transmembrane charge movement.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Planetary and Space Science 26 (1978), S. 1081-1140 
    ISSN: 0032-0633
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Geosciences , Physics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Planetary and Space Science 28 (1980), S. 443-447 
    ISSN: 0032-0633
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Geosciences , Physics
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Planetary and Space Science 23 (1975), S. 541-549 
    ISSN: 0032-0633
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Geosciences , Physics
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Planetary and Space Science 35 (1987), S. 997-1008 
    ISSN: 0032-0633
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Geosciences , Physics
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Planetary and Space Science 30 (1982), S. 5-28 
    ISSN: 0032-0633
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Geosciences , Physics
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Planetary and Space Science 17 (1969), S. 1505-1517 
    ISSN: 0032-0633
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Geosciences , Physics
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-2013
    Keywords: Cell volume Intracellular Ca2+ Patch clamp Urea Vascular smooth muscle cells Voltage gated Ca2+ channels hsk
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The present study was performed to elucidate the effects of urea on vascular smooth muscle cells (SMC). Addition of urea (20, 50, 100 mM) to physiological salt solution blunted the vasoconstrictory effect of phenylephrine (by 17, 25 and 30%, respectively) and of an increased extracellular K+ concentration (by 7, 14 and 19%, respectively) without affecting the basal tone of rabbit arterial rings. According to Fura-2 fluorescence in cultured SMC (A7r5), urea had no effect on basal intracellular calcium activity ([Ca2+]i), but significantly blunted the increase of [Ca2+]i following an increase of extracellular K+. Whole-cell patch-clamp studies revealed that the Ca2+ current through voltage-sensitive Ca2+ channels is significantly inhibited in the presence of urea. As evident from calcein fluorescence, addition of urea leads to sustained cell shrinkage. The effects of urea on vascular tone, [Ca2+]i activity, voltage-gated Ca2+ channels and cell volume are mimicked by addition of raffinose or NaCl. However, the cell shrinkage induced by urea is sustained, whereas the addition of equiosmolar NaCl is only transient and followed by a regulatory cell volume increase. Moreover, hypertonic NaCl increases, whereas urea decreases, the transcription of cell-volume-regulated kinase hsgk. In conclusion, urea leads to sustained shrinkage of vascular smooth muscle cells, which is followed by inhibition of voltage-gated Ca2+ channels, a decrease of [Ca2+]i and thus blunts the vasoconstrictory action of phenylephrine and increased extracellular K+ concentration.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-2013
    Keywords: Apoptosis ATP Cell death Cell shrinkage DNA fragmentation Lck56 Src-like kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Mitogenic factors are known to stimulate the Na+/H+-exchanger (NHE), leading to cytosolic alkalinization and/or cell swelling. Conversely, a hallmark of apoptosis is cell shrinkage and CD95-induced apoptosis has been reported to be paralleled by cytosolic acidification. To assess whether the CD95-receptor regulates NHE activity in Jurkat T-lymphocytes, we performed conventional BCECF fluorescence measurements and SNARF flow cytometric analysis (FACS). The recoveries from acidifications following application of butyrate or a NH3 pulse were both abolished by a specific NHE-inhibitor, HOE694, indicating that they fully depend on NHE activity. Thus they were taken as a measure of NHE activity. CD95-receptor stimulation caused a cytosolic acidification and blunted the recovery from acidification following application of butyrate or a NH3 pulse. Moreover, the NHE-dependent alkalinization following osmotic cell shrinkage was almost abolished by CD95-receptor stimulation. As apparent from the effect of osmotic cell shrinkage, inhibition of the NHE by CD95-receptor stimulation was absent in Lck56-deficient J-CaM1.6 cells and restored by retransfection of J-CaM1.6-cells with Lck56. CD95-receptor stimulation led within 4 h to a decrease of cellular ATP which could contribute to NHE inhibition. Treatment of Jurkat cells with the NHE inhibitor HOE694 accelerated CD95-induced DNA fragmentation. In conclusion, CD95-receptor stimulation inhibits NHE activity through a mechanism that depends directly or indirectly on the activation of the Src-like kinase Lck56. This effect contributes to CD95-induced cytosolic acidification, DNA fragmentation and cell shrinkage.
    Type of Medium: Electronic Resource
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