| Autor: |
Junankar, Pauline R., Karjalainen, Ari, Kirk, Kiaran |
| Předmět: |
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| Zdroj: |
Cellular Physiology & Biochemistry (Karger AG); 2004, Vol. 14 Issue 3, p143-154, 12p, 7 Graphs |
| Abstrakt: |
The pathways for the efflux of K+ from osmotically-swollen HTC rat hepatoma cells were investigated using 86Rb+ as a tracer for K+. Exposure of HTC cells to a hypotonic solution (< 250 mOsm kg-1) resulted in a transient efflux of 86Rb+ that reached a maximal value after ∼1 min, and inactivated within 3 min. This initial 86Rb+ efflux was inhibited by charybdotoxin, clotrimazole and Ba2+, but not by apamin or paxilline, consistent with it being via an intermediate conductance Ca2+-activated K+ channel. For cells exposed to an extracellular osmolality < 180 mOsm kg-1 there was an additional 86Rb+ efflux component which was slower to activate, taking 4 - 6 min to reach a maximum, and remaining active for > 20 min. The second 86Rb+ efflux component was not inhibited by K+ channel blockers but was inhibited by the anion channel blockers, tamoxifen, 5-nitro-2-(3-phenylpropylamino)benzoicacid (NPPB) and niflumate. The time-courses for its activation and inactivation, as well as its dependence on the extracellular osmolality, were very similar to those observed for the hypotonically-activated efflux of the organic osmolyte, taurine. The data are consistent with the second component of 86Rb+ efflux and the efflux of taurine from osmotically-swollen cells occurring via a common pathway having a marked selectivity for taurine over 86Rb+. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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