Mechanisms of XXXX -induced rise in cytoplasmic @entity460 concentrations in Madin Darby @entity235 kidney (MDCK) cells.

@entity11329 @entity671 @entity5897 @entity2426 @entity235 @entity3281 @entity593 @entity4385 @entity15130 @entity460 @entity141
The effect of @entity5897 on intracellular @entity460 levels ([ @entity141 ]i) in Madin Darby @entity235 kidney (MDCK) cells was studied using @entity593 as the @entity141 indicator. @entity5897 increased [ @entity141 ]i dose-dependently at concentrations of 5-100 microM. The [ @entity141 ]i transient consisted of an initial rise, a gradual decay and an elevated plateau (220 s after addition of the drug). Removal of extracellular @entity141 partly reduced the @entity5897 response. @entity3281 quench of @entity593 fluorescence confirmed that @entity5897 induced @entity141 influx. The @entity5897 -sensitive intracellular @entity141 store overlapped with that sensitive to @entity2426 , an inhibitor of the endoplasmic reticulum @entity141 pump, because 20 microM @entity5897 depleted the @entity2426 (1 microM)-sensitive store, and conversely, @entity2426 abolished @entity5897 -induced internal @entity141 release. @entity5897 (20-50 microM) partly inhibited the capacitative @entity141 entry induced by 1 microM @entity2426 , measured by depleting intracellular @entity141 store in @entity141 -free medium followed by addition of 10 mM @entity15130 . @entity5897 induced capacitative @entity141 entry on its own. Pretreatment with 0.1 mM La3+ partly inhibited 20 microM @entity5897 -induced @entity3281 quench of @entity593 fluorescence and [ @entity141 ]i rise, suggesting that @entity5897 induced @entity141 influx via two pathways separable by 0.1 mM @entity11329 . @entity5897 -induced internal @entity141 release was not altered when the cytosolic level of @entity671 (IP3) was substantially inhibited by the phospholipase C inhibitor @entity4385 .
