BACKGROUND: @entity1289 ( @entity1289 ) inhibitors have been reported to reduce the response to @entity1307 ( @entity1307 ) administration in chronic hemodialysis @entity1 , but the mechanism for this effect has not yet been clarified. To clarify the mechanism of @entity1289 inhibitors- and @entity7743 antagonist-induced @entity417 in hemodialysis @entity1 , we examined the effect of @entity1289 inhibitors and @entity7743 receptor antagonist on burst-forming units-erythroid (BFU-E) in the peripheral blood of hemodialysis @entity1 and healthy controls in vitro. METHODS: Peripheral blood mononuclear cells (PBMNCs) were isolated by gradient centrifugation from 10 @entity1 on regular hemodialysis and 7 healthy control volunteers. A colony assay of hematopoietic progenitors was performed using the methylcellulose culture system. PBMNCs of 1 or 2 x 10(5) were plated in a medium containing @entity1307 with various concentrations of @entity1289 inhibitors or @entity7743 receptor antagonist and incubated for 14 days. Colonies of BFU-E were counted under an inverted microscope. RESULTS: The PBMNCs from the chronic hemodialysis @entity1 formed fewer BFU-Es than those from healthy volunteers. @entity7743 receptor antagonist in both healthy volunteers and hemodialysis @entity1 suppressed the number of BFU-Es. The @entity1289 inhibitors produced a smaller effect than the @entity7743 receptor antagonist. CONCLUSION: @entity7743 receptor blockade can directly inhibit erythropoiesis in vitro.

Effects of an angiotensin II receptor antagonist and XXXX inhibitors on burst forming units-erythroid in chronic hemodialysis @entity1 .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity1289 :: ('1636', 'Gene') :: ['ACE', 'Angiotensin-converting enzyme'] @entity417 :: ('MESH:D000740', 'Disease') :: ['anemia'] @entity1307 :: ('2056', 'Gene') :: ['erythropoietin', 'EPO'] @entity7743 :: ('185', 'Gene') :: ['angiotensin II type 1 (AT1) receptor', 'AT1']
@entity1289 :: (1636,Gene) :: ['angiotensin-converting enzyme']
