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Comparative pharmacology of endothelium‐derived relaxing factor, nitric oxide and prostacyclin in platelets
Author(s) -
Radomski M.W.,
Palmer R.M.J.,
Moncada S.
Publication year - 1987
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1987.tb11310.x
Subject(s) - prostacyclin , platelet , endothelium derived relaxing factor , chemistry , nitric oxide , pharmacology , endothelium , superoxide , endogeny , superoxide dismutase , biochemistry , endocrinology , medicine , enzyme , organic chemistry
1 The pharmacological effects of endothelium‐derived relaxing factor (EDRF), nitric oxide (NO) and prostacyclin on human and rabbit platelets were examined. 2 EDRF is released from porcine aortic endothelial cells, cultured on microcarriers and treated with indomethacin, in sufficient quantities to inhibit platelet aggregation induced by 9,11‐dideoxy‐9α,11α‐methano epoxy‐prostaglandin F 2α (U46619) and collagen. 3 The anti‐aggregating activity of EDRF was potentiated by M&B 22948, a selective inhibitor of cyclic GMP phosphodiesterase, and by superoxide dismutase (SOD) and was inhibited by haemoglobin and Fe 2+ . 4 Both NO and prostacyclin inhibited platelet aggregation. 5 The anti‐aggregatory activity of NO, but not that of prostacyclin, was potentiated by M&B 22948 and by SOD and was inhibited by haemoglobin and Fe 2+ . Thus NO is a potent inhibitor of platelet aggregation whose activity on platelets mimics that of EDRF. 6 It is likely that the inhibitory effect of NO on platelets represents the action of endogenous EDRF and therefore this substance, together with prostacyclin, is a regulator of platelet‐vessel wall interactions.