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Erythropoietin Production by Fetal Mouse Liver Cells in Response to Hypoxia and Adenylate Cyclase Stimulation^*

Physiologisches Institut der Universität Zürich CH-8057 Zurich, Switzerland
Physiologisches Institut der Medizinischen Hochschule Lübeck D-2400 Lübeck, West Germany
Institut für Physiologie der Universität Regensburg D-8400 Regensburg, West Germany

Address correspondence and requests for reprints to: Dr. Armin Kurtz, Physiologisches Institut der Universität Zurich Irchel, Winterthurerstrasse 190, CH8057 Zürich, Switzerland.

Abstract

This study was done to investigate aspects of control of extrarerial erythropoietin (Ep) production. To this end we studied the effects of three stimuli of renal Ep production in the adult, i.e. hypoxia, cobalt, and activation of adehylate cyclase on Ep generation by cultured fetal mouse liver cells. The fetal liver was taken as a model for extrarenal Ep production because this organ is considered the predominant site of extrarenal Ep production. We found that Ep production by the cells increased as the oxygen concentration was decreased in the incubation atmosphere from 20% to 1%. Cobalt (10^–4–10^–5 M) had no effect on Ep production. Activation of adenylate cyclase by forskolin (10^–5 M) or isoproterenol (10^–6 M) greatly enhanced Ep production. These findings indicate that the Ep-stirriulating effect of cobalt is specific for the kidney. However, oxygen depletion and activation of adenylate cyclase seem to be more general stimuli in Ep-producing cells. Furthermore we found that Ep production in hypoxia correlated with lactate formation in the cultured liver cells. This finding suggests that Ep production in fetal livers under hypoxic conditions parallels the shift from aerobic to anaerobic cellular energy metabolism. (Endocrinology 118: 567–572, 1986)

Footnotes

^* This work was partly supported by Grant NF 3.023-0.84 from the Swiss National Science Foundation.

Received August 30, 1985.

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