Adenylate cyclase system of differentiating erythroid cells
Setchenska, M.S.
Acta Physiologica et Pharmacologica Bulgarica 16(2): 3-10
1990
ISSN/ISBN: 0323-9950 PMID: 2281799 Document Number: 347948
The review provides a survey of current knowledge about the changes in hormone-sensitive adenylate cyclase complex of erythroid cells. The basal enzyme activity decreases continuously during differentiation and maturation. Guanine nucleotides (GTP and GMP-P (NH)P) increase the adenylate cyclase activity of both early and late rabbit bone marrow erythroblasts. The stimulating effect of the .beta.2-adrenergic drugs such as L-isoprenaline is limited to the immature cells. L-noradrenaline a .beta.1-agonist is inactive. The lack of response of non-dividing rabbit erythroblasts to .beta.-adrenergic stimuli is not due to loss of .beta.-receptors during differentiation, but to a decrease in the effectiveness of the coupling between the components of the system: receptor-guanine nucleotide regulatory protein-catalytic subunit. Prostaglandins E1 and E2 consistently enhance adenylate cyclase activity of erythroblasts on different stages of development. Erythropoietin (0.2 U/ml) causes a transient increase in the activity of adenylate cyclase, which is maximal by 20 min incubation of the cells in the presence of the hormone and disappears within 4 hours. The magnitude of the response to erythropoietin depends on the stage of erythroid cell development and is inverse related to the extent of previous hormonal stimulation of the cell.