Chronic acidosis, chronic K deficiency, and chronic hyperfiltration all lead to similar parallel increases in Na/H antiporter and Na/3HCO3 cotransporter activities. These effects persist when the transporters are removed from the inducing environment, and thus represent memory effects. The effect of acidosis on the Na/H antiporter can be reproduced by preincubating cultured proximal tubule cells chronically in acid media, suggesting that low extracellular fluid pH is an important signal in acidosis. The specific extracellular signals in chronic K deficiency and chronic hyperfiltration have not been elucidated. The effect of acid preincubation on Na/H antiporter activity in cultured proximal tubule cells is dependent on protein synthesis and is associated with increased abundance of mRNA for the Na/H antiporter. The cell signalling pathways which mediate these effects have not been determined. However, the common response in chronic acidosis, chronic K deficiency, and chronic hyperfiltration to the demand for increased H transport, suggests that a common signalling pathway will be found in all these conditions.
|Original language||English (US)|
|Journal||Kidney International, Supplement|
|Publication status||Published - Jul 1991|
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