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Activation of the Na + ‐K + pump by hyposmolality through tyrosine kinase‐dependent Cl − conductance in Xenopus renal epithelial A6 cells
Author(s) -
Niisato Naomi,
Marunaka Yoshinori
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0417p.x
Subject(s) - chemistry , conductance , xenopus , physics , biochemistry , gene , condensed matter physics
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 ( I Na ), (2) Na + ‐K + pump activity, (3) basolateral Cl − conductance ( G b,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 G b,Cl , blocked the I Na by inhibiting the Na + ‐K + pump without any direct effect on amiloride‐sensitive Na + channels. Diminution of G b,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 G b,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 G b,Cl ; and (3) the PTK‐increased G b,Cl stimulates the Na + ‐K + pump. 6 This PTK‐activated G b,Cl ‐mediated signalling of hyposmolality is a novel pathway for stimulation of the Na + ‐K + pump.