Resolution of parameters in the equivalent electrical circuit of the sodium transport mechanism across toad skin.

Abstract

In amphibian epithelia, amiloride reduces net sodium transport by hindering the entry of sodium to the active transport mechanism, that is, by increasing the series resistance (Rser). Theoretically, therefore, analysis of amiloride-induced changes in potential differences and short-circuit current should yield numerical estimates of all the parameters in the equivalent electrical circuit of the sodium transport mechanism. The concept has been explored by analysis of such changes in toad skins (Xenopus laevis) bathed in hypotonic sulphate Ringer's, after exposure to varying doses of amiloride, or to amphotericin, dinitrophenol or Pitressin. The estimated values of Rser, of the electromotive force of the sodium pump (ENa), and of the shunt resistance (Rsh) were independent of the dose of amiloride employed. Skins bathed in hypotonic sulphate Ringer's exhibited a progressive rise in ENa. Amphotericin produced a fall in Rser, while dinitrophenol caused a fall in ENa; washout of the drugs reversed these effects. Pitressin produced a fall in both Rser and Rsh, with a rise in ENa. These results are in accord with earlier suggestions regarding the site(s) of action of these agents.