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.

下丘脑神经元产生的精氨酸加压素（AVP）释放到循环系统中，以刺激肾脏吸收水分并在失血后恢复水分平衡。缺乏这种抗利尿激素的患者患有中枢性尿崩症。我们观察到许多此类患者贫血，并询问AVP是否可能在红细胞（RBC）产生中起作用。我们发现，所有三个AVP受体均在人类和小鼠造血干细胞和祖细胞中表达。AVPR1B似乎在调节人类和小鼠细胞的红细胞生成中起着最重要的作用。AVP会增加促红细胞生成素（EPO）的作用，从而增加信号转导子和转录激活子5的磷酸化。亚致死剂量照射后，与对照组大鼠相比，AVP缺陷型的Brattleboro大鼠表现出RBC数量的恢复延迟。在贫血的小鼠模型（由出血，辐射或循环红细胞破坏增加引起）中，AVP增加了循环红细胞的数量，而与EPO无关。在这些模型中，AVP似乎可以开始补充外周血细胞，直到EPO能够接管为止。我们建议特定的AVPR1B激动剂可用于在出血，药物毒性或化疗后诱导快速的RBC产生。