Membrane-metabolic coupling and ion homeostasis in anoxia-tolerant and anoxia-intolerant hepatocytes.

KRUMSCHNABEL G, BIASI C, SCHWARZBAUM PJ, WIESER W

AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY, INTEGRATIVE AND COMPARATIVE PHYSIOLOGY

AMER PHYSIOLOGICAL SOC

Año: 1995 p. 614 - 620

0363-6119

relationship between membrane function and energy metabolismwas studied in rainbow trout hepatocytes, an anoxiaintolerantcell system, and compared with the situation inhepatocytes from the goldfish, a typical anoxia-tolerant species.In trout hepatocytes, under normoxia and under chemicalanoxia, inhibition of ATP consumption by the Na+ pumpinduced a decrease in ATP production of the same magnitude.In response to chemical anoxia, total ATP production wasreduced to 15% and Na+ pump activity to 22% of the controlrate under normoxia. Measurement of the cellular ATPcontent under these conditions revealed that, despite thereduction in Na+ pump activity, the cells became rapidlydepleted of ATP, with the time course of this process resemblingthat observed in the anoxic rat hepatocyte. This is incontrast to the responses of goldfish hepatocytes, where,during chemical anoxia, 1) inhibition of the Na+ pump did notlead to a corresponding reduction in ATP production and 2)ATP levels, after a transient decrease, stabilized at a newsteady state. To investigate the consequences of chemicalanoxia on ion homeostasis, efflux and uptake rates of K+ weredetermined simultaneously. In the trout cells, chemical anoxialed to a decoupling of influx and efflux rates, the latterexceeding the former three- to eightfold. In contrast, goldfishhepatocytes were able to preserve ion homeostasis by aconcerted decrease in Rb+ uptake and K+ efflux, so that thenet flux of K+ was always close to zero. In neither species didchemical anoxia induce a change in pump density. Otherpotential control mechanisms are briefly discussed.sodium pump; rubidium uptake; potassium efflux;