Loss of K+ homeostasis in trout hepatocytes during chemical anoxia: a screening study for potential causes and mechanisms

KRUMSCHNABEL G, FRISCHMANN M, SCHWARZBAUM PJ, WIESER W

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS

ELSEVIER SCIENCE INC

Año: 1998 p. 199 - 206

0003-9861

In isolated trout hepatocytes intoxication with CN2(chemical anoxia) leads to a rapid breakdown of K1homeostasis. In the present study an attempt has beenmade to identify the causes and mechanisms underlyingthis phenomenon. Our results indicate that neitherCa21 elevation nor cell swelling, both of whichoccurred during chemical anoxia and could be preventedby exposure to Ca21 chelating agents or tohyperosmotic conditions, respectively, is solely responsiblefor the breakdown of K1 homeostasis. Froma number of inhibitors of dissipative K1 fluxes tested,only BaCl2, an inhibitor of voltage-gated K1 channels,proved to be effective in significantly reducing K1 effluxduring chemical anoxia. The KCl cotransporterknown to be involved in regulatory volume decreaseafter hypoosmotic shock does not seem to be activatedduring CN2-induced cell swelling. © 1998 A