• 1 January 1981
    • journal article
    • research article
    • Vol. 42  (2) , 277-283
Abstract
Angiotensin II (At II) in the concentration range of 10-5-5 .times. 10-7 M inhibited active and passive erythrocyte-antibody (EA) rosette formation on monolayers of rat peritoneal macrophages (PM) but stimulated it in the range of 10-7-10-8 M. Cytochalasin B (CB) and vinblastine (Vb) inhibited the dose-dependent biphasic AT II effect on macrophage Fc receptor (FcR) expression. The hormone acts on the last step of rosette formation, i.e., on the binding of sheep red blood cells (SRBC) but does not interfere with the binding of 125I-Ig to FcR. At II influence on macrophage rosette formation can be modified by changes in the FcR-Ig complex density on the target cell surface, by the nature of the Ig (sub)classes involved in rosette formation and by the biological properties of rosette-forming corpuscular antigen. Apparently, At II exerts its effect on the contractile elements associated with the macrophage cytoskeleton.