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Regulation of erythropoiesis in the fetus and newborn.

The present concept of the regulation of erythropoiesis is based on the theory that a humoral factor, erythropoietin, stimulates red cell production through its effects on the erythropoietin sensitive stem cell, on DNA synthesis in the erythroblast, and on the release of reticulocytes (Gordon and Zanjani, 1970; Hodgson, 1970). Erythropoietin production is regulated by the difference between oxygen supply and demand within the oxygen sensitive cells in the kidney. As a response to hypoxia, a factor called erythrogenin is produced in the kidney. This factor acts on a serum substrate to generate an active humoral factor, the erythropoietic stimulating factor (ESF) or erythropoietin (Gordon, 1971), increased amount of which leads to increased red cell production. Many details in this theory are still a matter of controversy, as for example where in the kidney erythrogenin is produced, where the active ESF is generated, whether the kidney is the sole site of 02-tension registration and of erythrogenin production, and whether the active ESF is the only factor involved in the regulation of red cell production. Some data, for instance, indicate a more complicated model, and an erythropoietic inhibitory factor has been postulated whereby increased erythropoiesis could also result from a decrease of the inhibiting factor (Krzymowski and Krzymowska, 1962; Skjoelaaen and Halvorsen, 1971; Lindemann, 1971).