AJP - Renal Physiology, Vol 251, Issue 4 662-F670, Copyright © 1986 by American Physiological Society
Control of transepithelial Na+ transport and Na-K-ATPase by oxytocin and aldosterone
M. Girardet, K. Geering, H. P. Gaeggeler and B. C. Rossier
Short- and long-term effect of oxytocin on Na+ transport and Na-K-ATPase
biosynthesis in the toad bladder, and the potential interaction of this
hormone with aldosterone have been studied, leading to the following
observations. An early Na+ transport response (oxytocin, 50 mU/ml) peaked
at 10-15 min of hormone addition. At maximal stimulation a three- to
fourfold increase in Na+ transport was observed, a sustained Na+ transport
response (about two-fold control base line) was observed as long as the
hormone was present in the medium and for up to 20 h of incubation.
Pretreatment for 30 min with actinomycin D (2 micrograms/ml) did not
inhibit the early response, but significantly impaired the sustained
response, suggesting that de novo protein synthesis was required. The
simultaneous addition of the two hormones led within 60 min to a marked
potentiation of the action on Na+ transport. This synergism could be
mimicked by exogenous cyclic adenosine monophosphate (cAMP). Oxytocin alone
(18 h exposure, 50 mU/ml) increased the relative rate of synthesis of both
alpha and beta subunits of Na-K-ATPase (1.9- and 1.6-fold, respectively; P
less than 0.05), whereas aldosterone (80 nM) increased the relative rate of
synthesis of the same subunits (2.6- and 2.2-fold, respectively; P less
than 0.02). Finally, in contrast to what was observed at the physiological
level, the interaction of oxytocin and aldosterone did not lead to a
similar potentiation at the biochemical level, i.e., induction of
Na-K-ATPase biosynthesis (2.7- and 2.9-fold, for alpha and beta subunits,
respectively; P less than 0.025).
