Activation of the Na+-K+ pump by hyposmolality through tyrosine kinase-dependent Cl- conductance in Xenopus renal epithelial A6 cells
| Autor: | N, Niisato, Y, Marunaka |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
animal structures
Blotting Western Osmolar Concentration Epithelial Cells Original Articles Protein-Tyrosine Kinases Kidney Amiloride Xenopus laevis Hypotonic Solutions Chloride Channels Nitrobenzoates Animals Tyrosine Enzyme Inhibitors Phosphorylation Sodium-Potassium-Exchanging ATPase Diuretics Ouabain Cells Cultured |
| Zdroj: | The Journal of physiology. 518 |
| ISSN: | 0022-3751 |
| Popis: | 1. We studied the regulatory mechanism of Na+ transport by hyposmolality in renal epithelial A6 cells. 2. Hyposmolality increased (1) Na+ absorption, which was detected as an amiloride-sensitive short-circuit current (INa), (2) Na+-K+ pump activity, (3) basolateral Cl- conductance (Gb,Cl), and (4) phosphorylation of tyrosine, suggesting an increase in activity of protein tyrosine kinase (PTK). 3. A Cl- channel blocker, 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), which abolished Gb, Cl, blocked the INa by inhibiting the Na+-K+ pump without any direct effect on amiloride-sensitive Na+ channels. Diminution of Gb,Cl by Cl- replacement with a less permeable anion, gluconate, also decreased the hyposmolality-increased Na+-K+ pump activity. 4. The PTK inhibitors tyrphostin A23 and genistein induced diminution of the hyposmolality-stimulated Gb,Cl, which was associated with attenuation of the hyposmolality-increased Na+-K+ pump activity. 5. Taken together, these observations suggest that: (1) hyposmolality activates PTK; (2) the activated PTK increases Gb,Cl; and (3) the PTK-increased Gb,Cl stimulates the Na+-K+ pump. 6. This PTK-activated Gb,Cl-mediated signalling of hyposmolality is a novel pathway for stimulation of the Na+-K+ pump. |
| Databáze: | OpenAIRE |
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