Cell membrane potential and resistance in liver.

Abstract

Isolated segments of mouse liver were placed in a Perspex bath, through which physiological saline solutions of varying composition were circulated. Two microelectrodes were inserted in different liver cells under microscopic control allowing measurement of distance between the 2 microelectrode tips. Current pulses were injected through 1 of these electrodes, causing electrotonic potential changes in nearby cells by current spread through intercellular junctions. These electrotonic potential changes were recorded with the 2nd microelectrode. The spatial decrement of the amplitude of the electrotonic potential changes and their dependence on extracellular ion concentrations were analyzed by 3-dimensional cable analysis, modified to account for the geometry of the tissue. During exposure to control solution the mean resting cell membrane potential was -37 mV, the space constant for intracellular current spread (.lambda.3 = .sqroot.Rm/.chi.Ri) was 390 .mu.m and Ri, a measure which includes the intracellular resistivity and the junctional resistances, was 1.4 k?cm. From these values, and an estimate of tissue cell membrane density (.chi.) obtained by others, the specific membrane resistance (Rm) was 5.1 k?cm2. Replacement of extracellular Na+ by K+ resulted in a large depolarization and a large decrease in the membrane resistance. Replacement of extracellular Na+ by choline resulted in a small transient hyperpolarization and a small increase in the membrane resistance. Replacement of extracellular Cl- by methylsulfate or sulfate or of NaCl by sucrose resulted in a small transient depolarization and a large increase in the membrane resistance. Glucagon (10-7 M) and adrenaline [epinephrine] (10-5 M) evoked membrane hyperpolarization and reduction of membrane resistance (Rm). The resting membrane ion conductance consists of 3 components, Cl conductance (GCl), GK and GNa. The results suggest that GCl > GK > GNa. Changes in extracellular ion concentrations specifically alter the permeability properties of the cell membrane. The glucagon action can be partly explained by an increase in GK.