Abstract
Ureter-ligated rats, whose blood urea nitrogen concentration equalled that of nephrectomized animals, responded nearly like normal controls to bleeding or phenylhydrazine anemia, and erythropoietin was demonstrated in their plasma. This eliminates the urea retention as a depressing factor of erythropoiesis in uremia.
Bilaterally nephrectomized or mercury-bichloride poisoned rats did not respond significantly to anemic stimuli. No erythropoietin was found in the plasma of bled or phenylhydrazine-poisoned nephrectomized rats. The injection of erythropoietin produced significant increases in the erythropoiesis of nephrectomized or mercury-bichloride poisoned rats, but the response was substantially smaller than in ureter-ligated or sham-operated animals.
The presence of funtioning renal (tubular) tissue appears to be necessary for a normal erythropoietic response. Renal formation of erythropoietin with a rapid normal turnover, or the accumulation of an inhibitor, distinct from urea and normally inactivated by the kidneys, are discussed as possible mechanisms.
