Abstract
A humoral regulation of erythropoiesis was proposed by Carnot and Deflandre in 1906 when they demonstrated that plasma from anemic rabbits produced an increase in erythrocyte levels in blood when injected into recipient rabbits [1]. This proposal of a humoral control of erythropoiesis was not substantiated until the work of Hjort in 1936 [2] and Erslev in 1953 in which these investigators found that large volumes of plasma from rabbits following bleeding produced a marked reticulocytosis when injected into recipient animals. This reawakened interest in the search for a hormone which might regulate erythropoiesis and this area of research was placed on a more firm basis with the early experiments by Reissmann et al. [4] in which he found that one member of a parabiotic pair of rats exposed to hypoxia produced bone marrow erythroid hyperplasia in both rats. This implicated a humoral factor which passed from the hypoxic partner to the non-hypoxic partner to stimulate erythropoiesis. This hormone was given the name “erythropoietin” (Epo) by Bonsdorff and Javalisto [5] in 1948. Several investigators were interested in the organ which produces erythropoietin. Jacobson et al. [6] found that bilaterally nephrectomized rats exposed to bleeding or cobalt failed to elevate erythropoietin plasma levels.
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