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1. The effect of stimulation of hepatic - and -sympathetic receptors on the membrane potential of liver cells was studied utilizing the isolated perfused dog liver. In this preparation, potentials are maintained close to their normal values (around -50 mV) for several hours.

2. The administration of adrenaline (0·5 µM) caused an immediate depolarization, which reached 23 mV in 2 min. The potential gradually returned to base line levels in less than 20 min. A slight hyperpolarization often followed, despite a fall in the K content of the tissues. Similar results could be obtained with a lower concentration (0·1 µM) of adrenaline.

3. Potential changes after adrenaline injection are not altered by prior inhibition of the Na pump by ouabain. The adrenaline induced depolarization may be attributed to an increase in P_Na and the repolarization to a decrease in P_Na. An electrogenic mechanism does not seem to be involved.

4. Administration of the -sympathomimetic agent isoprenaline (1 µM) is followed by hyperpolarization, the potential increasing from -45·7 ± 1·5 to -55·0 ± 2·7 mV. Isoprenaline also slows the potential drop produced by ouabain. The action of isoprenaline may be explained by a reduction in permeability to Na.

5. Adrenaline also produces hyperpolarization in the presence of an -blocking agent, phenoxybenzamine. In the presence of a -blocking agent, propranolol, it causes more prolonged depolarization.

6. In the dog, the effect of -stimulation appears to be a rapid increase in permeability to Na, producing depolarization and of Na for K exchange. Stimulation of -receptors results in a slower decrease in P_Na and hyperpolarization. The combination of these two effects could explain the depolarization followed by repolarization produced by adrenaline.