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Mediators from mast cells and basophils account for most of the signs and symptoms of anaphylaxis. Histamine is a bronchoconstrictor and causes vasodilatation and increased vascular permeability. The cardiovascular effects of histamine occur through action on both H1 and H2 receptors. Numerous studies have demonstrated that the hypotensive effect of histamine infusion can only be blocked by the use of an H1 antihistamine combined with the H2 antihistamine cimetidine. It is unknown whether other H2 antihistamines would also be effective since these have not been studied. Increased serum histamine and tryptase levels have been demonstrated in patients with anaphylaxis. Leukotrienes are also likely to contribute to the anaphylactic syndrome. They cause bronchconstriction and increased vascular dilatation and permeability. Finally, it is likely that increased nitric oxide production occurs in human anaphylaxis, as has been demonstrated in animals. Nitric oxide is a potent vasodilator. L-arginine is converted to nitric oxide as histamine binds to H1-receptors during phospholipase-C-dependent calcium mobilization. Tumor necrosis factor released from mast cells also induces nitric oxide production. Nitric oxide production may be responsible for vasopressor-resistant cases of anaphylactic hypotension.