ALDOSTERONE-INDUCED INCREASE IN THE ABUNDANCE OF NA+ CHANNEL SUBUNITS

The highly selective, amiloride-blockable Na+ channel is a major targe t to the natriferic action of the mineralocorticoid aldosterone. This rat epithelial Na+ channel (rENaC) has been recently cloned from colon and is composed of three homologous subunits denoted alpha-, beta-, a nd gamma-rENaC (C. M. Canessa, L. Schild, G. Buell. B. Thorens, I. Gau tschi, J.-D. Horisberger, and B. C. Rossier. Nature Lend. 367: 463-467 , 1994). We have tested the effects of corticosteroids on the abundanc e of mRNA coding for each subunit in kidney cortex and distal colon. C hronic treatment of rats with aldosterone or dexamethasone evoked in k idney cortex a small induction of alpha-rENaC and no change in beta- a nd gamma-rENaC. In distal colon, however, beta- and gamma-rENaC were s trongly induced by either aldosterone or dexamethasone, whereas alpha- rENaC was constitutively expressed. Most of the aldosterone-induced in crease in beta- and gamma-rENaC mRNA took place during 3-24 h after pl asma aldosterone was elevated. A similar differential induction of rEN aC subunits in kidney and colon was also evoked by a Na+-free diet. Th e effects of salt deprivation were reversed by resalinating rats with a half time of <2 h, suggesting a high turnover rate of at least beta- and gamma-rENaC. The data are consistent with the possibility that in duction of channel subunits contributes to the chronic but not the acu te response to aldosterone in the colon. Such a mechanism is not likel y to play a major role in cortical collecting ducts.