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1. The electrical response of isolated toad skins to the presence of 4 x 10^-5 M noradrenaline in the inner medium has been studied.

2. When skins were bathed in Ringer solution, noradrenaline initiated a partial depolarization of the skin potential (inside surface becoming less positive) followed by a hyperpolarization; however, noradrenaline depolarized skins in sulphate Ringer.

3. The origin of the hyperpolarizing phase of the response to noradrenaline was studied by comparing the size of perturbations in the skin potential, produced by identical changes in external sodium, external chloride or internal potassium concentrations, before and during the response to noradrenaline.

4. Measurements of skin conductance were made in different sulphate media in order to estimate the magnitudes of the conductance of the shunt pathway through the skin and the conductance of the pathway for actively transported sodium ions.

5. Interpretation of both the variations in the perturbations of skin potential and the skin conductance measurements led to the conclusion that the hyperpolarizing phase of the response to noradrenaline was generated by an increase in the sodium to chloride permeability ratio for the outer barrier. It was considered that other evidence was compatible with this view.

6. Similar experimental methods were employed to study the action of antidiuretic hormone (ADH) and an elevated external concentration of calcium on the outer barrier. It was found that ADH increased the sodium to chloride permeability ratio whereas calcium decreased it. The separate actions of ADH and calcium on the sodium permeability of the outer barrier did not interfere apparently with the subsequent ability of noradrenaline to increase the sodium to chloride permeability ratio for this barrier in the skin.