The transmembrane electrical potential gradient (E(m)) has been measured in hepatocytes from intact anesthetized rats using conventional intracellular microelectrodes under a variety of conditions. E(m) measurements in control animals were normally distributed around a mean of -35.5 ± 4.6 mV (SD) with a coefficient of variation (CV) of 13.1% and a range of -26 to -54 mV. In individual livers, however, measurements of E(m) at a given point in time exhibited little cell-to-cell variation (cv of 4.5%). The E(m) was noted to fluctuate spontaneously over time and to change consistently in response to a variety of physiological stimuli including fasting (depolarization to -28.5 ± 3.8 mV) and infusion of glucagon in physiological amounts (hyperpolarization to -45.0 ± 1.8 mV). Hepatocyte E(m) abruptly depolarized (2-5 mV) after an intravenous bolus of taurocholate (3 μmol) or alanine (45 μmol), suggesting that both solutes exhibit electrogenic uptake. The E(m) returned to or below preinfusion values within 5 min. Continued infusion of alanine (10.8 μmol/min), but not taurocholate (810 nmol/min), caused a sustained and unexpected hyperpolarization of E(m) of 8.2 ± 3.1 mV that lasted at least 60 min. In separate studies, alanine administration did not alter the biliary excretion of a taurocholate load. Taken together, these observations demonstrate that rat hepatocytes in situ are tightly coupled electrically and that physiological stimuli, including fasting, glucagon, and sodium-coupled solute uptake can change E(m) considerably over time. The late hyperpolarization of E(m) caused by alanine appears to offset the rise in intracellular Na+ associated with alanine uptake and preserve the Na+ electrochemical gradient such that Na+-coupled taurocholate transport is maintained.
|Original language||English (US)|
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|State||Published - Jan 1 1987|
ASJC Scopus subject areas
- Physiology (medical)