Pflügers Archiv

, Volume 428, Issue 5–6, pp 552–560 | Cite as

Effects of urea on K+ fluxes and cell volume in perfused rat liver

  • Christian Hallbrucker
  • Stephan vom Dahl
  • Markus Ritter
  • Florian Lang
  • Dieter Häussinger
Heart, Circulation, Respiration and Blood; Environmental and Exercise Physiology


Exposure of the perfused rat liver to a perfusate made hyperosmotic by the presence of 200 mmol l−1glucose led, as expected, to marked, transient hepatocellular shrinkage followed by volume-regulatory net K+ uptake. However, even after this volume-regulatory K+ uptake had ceased, the liver cells are still slightly shrunken. Withdrawal of glucose from the perfusate resulted in marked transient cell swelling, net K+ release from the liver and restoration of cell volume. However, when the Krebs-Henseleit perfusate was made hyperosmotic by the presence of urea (20–300 mM), there was no immediate decrease in liver mass, yet a slight and persistent cell shrinkage developing 2 min after the onset of exposure to urea. Surprisingly, urea induced concentration-dependent net K+ efflux from the liver and removal of urea net K+ reuptake from the inflowing perfusate. The urea (200 mM)-induced net K+ release resembled that observed following a lowering of the influent [NaCl]: making the perfusate hypoosmotic (245 mosmol l−1, by reducing influent [NaCl] by 30 mM) gave roughly the same K+ response as hyperosmotic exposure (505 mosmol/l) resulting from the presence of 200 mM urea. The urea-induced K+ efflux was not inhibited in the presence of ouabain (1 mM), or in Ca++-free perfusion, but was modified in the presence of quinidine (1 mM) or Ba++ (1 mM). The direction in which the liver was perfused had no effect on the urea-induced net K+ release. Electrophysiological studies showed that urea led to quinidine-sensitive hyperpolarization and increase in K+ selectivity of plasma membranes, suggesting opening of K+ channels in the hepatocyte plasma membrane in response to urea. The data suggest that urea, but not glucose, enters the hepatocyte as quickly as water. Furthermore, urea at high concentrations apparently leads to K+ efflux from the hepatocyte and cell shrinkage, possibly due to opening of K+ channels in the hepatocyte plasma membrane.

Key words

Perfused liver Cell volume regulation Urea K+ fluxes Membrane potential K+ channels Glucose 


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Copyright information

© Springer-Verlag 1994

Authors and Affiliations

  • Christian Hallbrucker
    • 1
  • Stephan vom Dahl
    • 1
  • Markus Ritter
    • 2
  • Florian Lang
    • 3
  • Dieter Häussinger
    • 1
  1. 1.Medizinische Universitätsklinik FreiburgFreiburgGermany
  2. 2.Physiologisches Institut der Universität InnsbruckInnsbruckAustria
  3. 3.Physiologisches Institut der Universität TübingenTübingenGermany

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