Cell membrane potential and resistance in liver.
1. 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 two micro-electrode tips. Current pulses were injected through one of these electrodes, causing electrotonic potential changes in nearby cells by current spread through intercellular junctions. These electrotonic potential changes were recorded with the second micro-electrode. The spatial decrement of the amplitude of the electrotonzpotential changes and their dependence on extracellular ion concentrations were analysed by three-dimensional cable analysis, modified to account for the geometry of the tissue. 2. During exposure to control solution the mean resting cell membrane potential was -37 mV, the space constant for intracellular current spread (lambda3 = square root of Rm/chrRi) was 390 micron and Ri, a measure which includes the intracellular resistivity and the junctional resistances, was 1.4 komegacm. From these values, and an estimate of tissue cell membrane density (chi) obtained by others, the specific membrane resistance (Rm) was calculated to be 5.1 komegacm2. 3. 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 methylsulphate or sulphate or of NaCl by sucrose resulted in a small transient depolarization and a large increase in the membrane resistance. 4. Glucagon (10(-7) M) and adrenaline (10(-5) M) evoked membrane hyperpolarization and reduction of membrane resistance (Rm). 5. The resting membrane ion conductance can be considered to consist of three components, Cl conductance (GCl), GK and GNa. The results suggest that GCl greater than GK greater than GNa. Changes in extracellular ion concentrations specifically alter the permeability properties of the cell membrane. The glucagon action can be explained in part by an increase in GK.
D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D002712:Chlorides / Q000494:pharmacology; D004553:Electric Conductivity; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D005934:Glucagon / Q000494:pharmacology; D066298:In Vitro Techniques; D008099:Liver / Q000166:cytology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology
D002712:Chlorides; D005934:Glucagon; D012964:Sodium; D011188:Potassium; D004837:Epinephrine