Loss of K+ homeostasis in trout hepatocytes during chemical anoxia: a screening study for potential causes and mechanisms.
In isolated trout hepatocytes intoxication with CN- (chemical anoxia) leads to a rapid breakdown of K+ homeostasis. In the present study an attempt has been made to identify the causes and mechanisms underlying this phenomenon. Our results indicate that neither Ca2+ elevation nor cell swelling, both of which occurred during chemical anoxia and could be prevented by exposure to Ca2+ chelating agents or to hyperosmotic conditions, respectively, is solely responsible for the breakdown of K+ homeostasis. From a number of inhibitors of dissipative K+ fluxes tested, only BaCl2, an inhibitor of voltage-gated K+ channels, proved to be effective in significantly reducing K+ efflux during chemical anoxia. The KCl cotransporter known to be involved in regulatory volume decrease after hypoosmotic shock does not seem to be activated during CN(-)-induced cell swelling.
Krumschnabel
G
G
Abteilung für Okophysiologie, Universität Innsbruck, Austria.
Frischmann
M E
ME
Schwarzbaum
P J
PJ
Wieser
W
W
D000693:Anaerobiosis; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015687:Cell Hypoxia; D003486:Cyanides / Q000506:poisoning*; D006019:Glycolysis; D006706:Homeostasis / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000502:physiology*; D017686:Oncorhynchus mykiss; D009994:Osmolar Concentration; D011188:Potassium / Q000502:physiology*
D003486:Cyanides; D011188:Potassium; D002118:Calcium