A role for the renin-angiotensin system in hematopoiesis

The effects of the renin-angiotensin system (RAS) on blood pressure regulation were first described in 1898 by the physiologist Robert Tigerstedt, following observations that blood pressure increased in anesthetized animals following the injection of kidney extracts.1–3 Since then, the RAS has been characterized extensively, not only for its roles in hypertension and atherosclerosis, but also for its relevance to the fields of diabetes, oncology, and hematology. It has been recently recognized that the RAS plays critical physiological roles beyond its originally recognized functions in cardiovascular and fluid homeostasis regulation. For example, in this issue of the journal, Heringer-Walther et al.4 investigated the effects of angiotensin-(1–7) on in vitro proliferation and in vivo engraftment of human hematopoietic progenitor cells. These authors reported that the angiotensin II (Ang II) metabolite, Ang-(1–7) positively stimulates the proliferation of CD34+ cord blood cells in vitro. They also demonstrated that coinjection of cord blood mononuclear cells with continuous post-transplantation supplementation of Ang-(1–7) drastically improved human hematopoietic progenitor engraftment. These results continue to highlight an important yet unappreciated role for RAS in regulating hematopoietic progenitor differentiation and self-renewal. Moreover, the use of Ang-(1–7), Ang II, or manipulation of Ang II receptor binding may have utility and clinical significance in bone marrow transplantation.