Abstract
The epithelial Na+ channel (ENaC) functions as the rate-limiting factor in aldosterone-regulated transcellular Na+ transport. In the study described here, the effect of aldosterone on ENaC mRNA levels, protein synthesis and benzamil-sensitive Na+ transport was investigated using primary cultures of immunodissected rabbit kidney connecting tubule and cortical collecting duct cells (CNT and CCD, respectively). After a lag time of 3 h, aldosterone caused transepithelial Na+ transport to increase, reaching maximal level of 260±44% after 16 h of incubation. The α, β and γ rabbit ENaC (rbENaC) mRNA levels, measured by semi-quantitative reverse transcriptase-polymerase chain reaction, were not changed by aldosterone during the first 3 h, but a twofold increase was apparent after 6 h; levels remained elevated for up to 16 h of incubation. Immunoprecipitation of [35S]methionine-labeled rbENaC revealed a rise in protein levels of the α and β subunits, but the protein level of the γ subunit remained constant. In conclusion, our data suggest that in rabbit CNT and CCD the early increase in Na+ transport caused by aldosterone is due to the activation or insertion of existing Na+ channels into the apical membrane, and that the late response is mediated by increased synthesis of the α and β rbENaC subunits.
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Received: 4 January 1999 / Received after revision: 2 March 1999 / Accepted: 18 March 1999
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Dijkink, L., Hartog, A., Deen, P. et al. Time-dependent regulation by aldosterone of the amiloride-sensitive Na+ channel in rabbit kidney. Pflügers Arch 438, 354–360 (1999). https://doi.org/10.1007/s004240050920
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DOI: https://doi.org/10.1007/s004240050920