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Inhibition of antigen-induced and anti-immunoglobulin-induced capping by hydrocortisone and propranolol
The redistribution of lymphocyte surface immunoglobulin (Ig) induced by anti-Ig antibody or bound sheep erythrocyte antigen (capping) was inhibited reversibly by hydrocortisone succinate (2 x 10(-4) M). Capping inhibition was also effected by cholesterol and progesterone, favoring the hypothesis that the effect was mediated through changes in the physical properties of the cell membrane rather than hormonal action. Capping was also inhibited by propranolol at concentrations where it may exert a local anesthetic as well as a beta-adrenergic blocking effect (2 x 10(-4) M). Since a fourfold excess of the beta agonist isoproterenol failed to restore capping in the presence of propranolol, the local anesthetic mode of action is most likely. Nitroprusside, an inhibitor of contraction in vascular smooth muscle and platelets, failed to inhibit capping.
The redistribution of lymphocyte surface immunoglobulin (Ig) induced by anti-Ig antibody or bound sheep erythrocyte antigen (capping) was inhibited reversibly by hydrocortisone succinate (2 x 10(-4) M). Capping inhibition was also effected by cholesterol and progesterone, favoring the hypothesis that the effect was mediated through changes in the physical properties of the cell membrane rather than hormonal action. Capping was also inhibited by propranolol at concentrations where it may exert a local anesthetic as well as a beta-adrenergic blocking effect (2 x 10(-4) M). Since a fourfold excess of the beta agonist isoproterenol failed to restore capping in the presence of propranolol, the local anesthetic mode of action is most likely. Nitroprusside, an inhibitor of contraction in vascular smooth muscle and platelets, failed to inhibit capping.
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