Inhibitory effects of relaxin on human basophils activated by stimulation of the Fc epsilon receptor. The role of nitric oxide.
This study investigates whether relaxin (RLX), a hormone previously shown to inhibit mast cell function and to stimulate endogenous nitric oxide (NO) biosynthesis, counteracts the activation of isolated human basophils stimulated with anti-IgE or phorbol ester, and, if so, whether NO is involved. RLX reduced dose-dependently the expression of the activation marker CD63, the release of histamine and the rise of intracellular Ca2+ levels which triggers granule release by stimulated basophils. RLX also blunts the ultrastructural signs of anaphylactic granule release. The effects of RLX appear to depend upon activation of Ca2+/calmodulin-dependent NO synthase and endogenous NO production. They were reproduced by the NO donor sodium nitroprusside (SNP) and were reverted by the NO synthase inhibitor N(omega)-monomethyl-L-arginine, or by the NO scavenger oxyhemoglobin, or by blocking the NO physiological target guanylate cyclase with ODQ. In conclusion, RLX appears to play a role in down-regulating basophil function upon immunologic and nonimmunologic activation.
D001491:Basophils / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D009569:Nitric Oxide / Q000276:immunology / Q000502:physiology*; D017455:Receptors, IgE / Q000096:biosynthesis* / Q000276:immunology; D012065:Relaxin / Q000494:pharmacology*
D017455:Receptors, IgE; D009569:Nitric Oxide; D012065:Relaxin