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Lack of angiotensin II–facilitated erythropoiesis causes anemia in angiotensin-converting enzyme–deficient mice

By Justin Cole, Dilek Ertoy, Hsinchen Lin, Roy L. Sutliff, Eric Ezan, Tham T. Guyene, Mario Capecchi, Pierre Corvol and Kenneth E. Bernstein

Abstract

While nephrologists often observe reduced hematocrit associated with inhibitors of angiotensin-converting enzyme (ACE), the basis for this effect is not well understood. We now report that two strains of ACE knockout mice have a normocytic anemia associated with elevated plasma erythropoietin levels. (51)Cr labeling of red cells showed that the knockout mice have a normal total blood volume but a reduced red cell mass. ACE knockout mice, which lack tissue ACE, are anemic despite having normal renal function. These mice have increased plasma levels of the peptide acetyl-SDKP, a possible stem cell suppressor. However, they also show low plasma levels of angiotensin II. Infusion of angiotensin II for 2 weeks increased hematocrit to near normal levels. These data suggest that angiotensin II facilitates erythropoiesis, a conclusion with implications for the management of chronically ill patients on inhibitors of the renin-angiotensin system

Topics: Article
Publisher: American Society for Clinical Investigation
Year: 2000
DOI identifier: 10.1172/jci10557
OAI identifier: oai:pubmedcentral.nih.gov:381466
Provided by: PubMed Central
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