AJP - Cell Physiology, Vol 248, Issue 1 102-C108, Copyright © 1985 by American Physiological Society

ARTICLES

Receptor occupancy vs. induction of Na+-K+-ATPase and Na+ transport by aldosterone

K. Geering, M. Claire, H. P. Gaeggeler and B. C. Rossier

In the urinary bladder of the toad Bufo marinus aldosterone (between 0.8 and 100 nM) stimulates Na+ transport [half-maximal induction concentration (K1/2) = 6.5 nM]. At low hormone concentrations (0.8-8 nM), the increase of Na+ transport between 0.75 and 2.5 h is accompanied by a fall in transepithelial resistance (R). Higher hormone concentrations (30-800 nM) induce an additional resistance-independent fraction of Na+ transport within 2.5-8 h. From 6 h on, aldosterone (between 0.2 and 20 nM) stimulates in the same tissue the biosynthesis rate of the alpha- and beta-subunits of Na+-K+-ATPase (K1/2 = 3 and 1.5 nM, respectively). New pump synthesis is thus not a prerequisite for the early mineralocorticoid response but might be linked to the late transport event. The mineralocorticoid response is usually ascribed to interaction with the higher affinity type 1 receptor. In the present study we show, however, that at least 55% of the overall Na+ transport response is linked to nuclear occupation of the lower affinity type 2 receptors [dissociation constant (Kd) = 50 nM, maximum number of binding sites (Nmax) = 315 fmol/mg protein]. Distinct aldosterone effects, such as the fall in R and the increase in Na+-K+-ATPase synthesis, are more closely related to occupation of type 1 receptors (Kd = 0.3 nM, Nmax = 23 fmol/mg protein). At maximal induction of these latter parameters, only about 20% of type 2 receptors are occupied. These results suggest that both types of aldosterone receptors are involved in the mediation of the full mineralocorticoid response: type 1 in the early and late and type 2 particularly in the late tissue response.

This article has been cited by other articles:

				J. Nielsen, T.-H. Kwon, J. Frokiaer, M. A. Knepper, and S. Nielsen Maintained ENaC trafficking in aldosterone-infused rats during mineralocorticoid and glucocorticoid receptor blockade Am J Physiol Renal Physiol, January 1, 2007; 292(1): F382 - F394. [Abstract] [Full Text] [PDF]

				V. Summa, D. Mordasini, F. Roger, M. Bens, P.-Y. Martin, A. Vandewalle, F. Verrey, and E. Feraille Short Term Effect of Aldosterone on Na,K-ATPase Cell Surface Expression in Kidney Collecting Duct Cells J. Biol. Chem., December 7, 2001; 276(50): 47087 - 47093. [Abstract] [Full Text] [PDF]

				S. DJELIDI, A. BEGGAH, N. COURTOIS-COUTRY, M. FAY, F. CLUZEAUD, S. VIENGCHAREUN, J.-P. BONVALET, N. FARMAN, and M. BLOT-CHABAUD Basolateral Translocation by Vasopressin of the Aldosterone-Induced Pool of Latent Na-K-ATPases Is Accompanied by {alpha}1 Subunit Dephosphorylation: Study in a New Aldosterone-Sensitive Rat Cortical Collecting Duct Cell Line J. Am. Soc. Nephrol., September 1, 2001; 12(9): 1805 - 1818. [Abstract] [Full Text] [PDF]

				A. G. Therien and R. Blostein Mechanisms of sodium pump regulation Am J Physiol Cell Physiol, September 1, 2000; 279(3): C541 - C566. [Abstract] [Full Text] [PDF]

				A. Shigaev, C. Asher, H. Latter, H. Garty, and E. Reuveny Regulation of sgk by aldosterone and its effects on the epithelial Na+ channel Am J Physiol Renal Physiol, April 1, 2000; 278(4): F613 - F619. [Abstract] [Full Text] [PDF]

				F. Verrey Early aldosterone action: toward filling the gap between transcription and transport Am J Physiol Renal Physiol, September 1, 1999; 277(3): F319 - F327. [Abstract] [Full Text] [PDF]

				M. BENS, V. VALLET, F. CLUZEAUD, L. PASCUAL-LETALLEC, A. KAHN, M. E. RAFESTIN-OBLIN, B. C. ROSSIER, and A. VANDEWALLE Corticosteroid-Dependent Sodium Transport in a Novel Immortalized Mouse Collecting Duct Principal Cell Line J. Am. Soc. Nephrol., May 1, 1999; 10(5): 923 - 934. [Abstract] [Full Text]