Abstract
Effects of noradrenaline (NA) on the membrane potential and the membrane resistance were studied in the guinea pig liver slices. The slices (2×2×6 mm) were prepared from the left lobe of the liver and superfused with Krebs solution. The mean membrane potential was -53.1mV. Electrotonic potentials were recorded in an extrapolar region of liver cells when current pulses were applied between two extracellular electrodes. It was shown that a liver slice had cable-like properties. The space constant was estimated to be 0.38 mm and the time constant 5.2 msec. Administration of NA (10-5M) caused initial depolarization followed by hyperpolarization and an reduction in the size of the electrotonic potentials, suggesting a reduction in the membrane resistance. The response to NA depended on the membrane potential, i.e., the depolarizing component of the biphasic response was larger with higher membrane potential, while the hyperpolarizing component was larger with lower membrane potential. Both components of the response were blocked by an α-blocker, phentolamine (1.5×10-5M), but not by a β-blocker, propranolol. The depolarizing component became smaller in a Na+-deficient and in a Cl-deficient solution, and was abolished in a solution lacking both Na+ and Cl-. These results may indicate that increases in Na+ and Cl- conductances may be responsible for the depolarizing component. The hyperpolarizing component was increase when the external K+ concentration was reduced, and the change in the eak potential with the external K+ concentration was larger in the presence of NA. In addition to these, the dependence of the response on the membrane potential and the reduction of the membrane resistance may suggest that the hyperpolarizing component of NA response is produced mainly by an increase in K+ conductance.
