Research ArticleANEMIA

Vasopressin stimulates the proliferation and differentiation of red blood cell precursors and improves recovery from anemia

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Science Translational Medicine  29 Nov 2017:
Vol. 9, Issue 418, eaao1632
DOI: 10.1126/scitranslmed.aao1632

The body’s stop-gap solution for anemia

Vasopressin is an antidiuretic hormone, whose best known functions are to promote water retention and maintain fluid balance. However, it also has other effects, and Mayer et al. discovered that these include stimulation of red blood cell maturation. By studying human patients with central diabetes insipidus (vasopressin deficiency) and a rat model that lacks vasopressin, the authors determined that this hormone acts in concert with erythropoietin but on a shorter time scale. Erythropoietin stimulates red blood cell production starting with early progenitors, which takes time, whereas vasopressin promotes maturation of intermediate red blood cell precursors and thus allows rapid recovery after blood loss while the new cells stimulated by erythropoietin are still maturing.


Arginine vasopressin (AVP) made by hypothalamic neurons is released into the circulation to stimulate water resorption by the kidneys and restore water balance after blood loss. Patients who lack this antidiuretic hormone suffer from central diabetes insipidus. We observed that many of these patients were anemic and asked whether AVP might play a role in red blood cell (RBC) production. We found that all three AVP receptors are expressed in human and mouse hematopoietic stem and progenitor cells. The AVPR1B appears to play the most important role in regulating erythropoiesis in both human and mouse cells. AVP increases phosphorylation of signal transducer and activator of transcription 5, as erythropoietin (EPO) does. After sublethal irradiation, AVP-deficient Brattleboro rats showed delayed recovery of RBC numbers compared to control rats. In mouse models of anemia (induced by bleeding, irradiation, or increased destruction of circulating RBCs), AVP increased the number of circulating RBCs independently of EPO. In these models, AVP appears to jump-start peripheral blood cell replenishment until EPO can take over. We suggest that specific AVPR1B agonists might be used to induce fast RBC production after bleeding, drug toxicity, or chemotherapy.

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