Chloride Conductance and P i Transport are Separate Functions Induced by the Expression of NaPi-1 in Xenopus Oocytes

Chloride Conductance and P i Transport are Separate Functions Induced by the Expression of... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Chloride Conductance and P i Transport are Separate Functions Induced by the Expression of NaPi-1 in Xenopus Oocytes

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Publisher
Springer-Verlag
Copyright
Copyright © Inc. by 1998 Springer-Verlag New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002329900394
Publisher site
See Article on Publisher Site

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.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Jul 1, 1998

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