Spasmogenic Mediators

Histamine, generated by decarboxylation of histidine, was the first mast cell mediator to be identified, and it is the sole preformed mediator in this functional class. It is bound to the proteoglycans of mast cell and basophil granules (5 and 1 mg/106 cells, respectively) (2.4,2.5). Histamine circulates at concentrations of about 300 pg/mL with a circadian maximum in the early morning hours (26). Histamine excretion exceeds 10 mg/24 hours; a small fraction is excreted as the native molecule, and the remainder as imidazole acetic acid or methyl histamine. Histamine interacts with specific H,, H2, and H3 receptors (2.7,28). H receptors predominate in the skin and smooth muscle; H2 receptors are most prevalent in the skin, lungs, and stomach and on a variety of leukocytes; and H 3 receptors predominate in the brain. The biologic response to histamine reflects the ratio of these receptors in a given tissue. H 1 histamine effects include contraction of bronchial and gut musculature, vascular permeability, pulmonary vasoconstriction, and nasal mucus production ( 29,30.). By its H2 pathway, histamine dilates respiratory musculature, enhances airway mucus production, inhibits basophil and skin (but not lung) mast cell degranulation, and activates suppressor T lymphocytes. Both H 1 and H2 actions are required for the full expression of pruritus, cutaneous vasodilation, and cardiac irritability ( 27). The H3 actions of histamine suppress central nervous system histamine synthesis. Increased levels of histamine have been reported in the blood or urine of patients with physical urticaria, anaphylaxis, systemic mastocytosis, and antigen-induced rhinitis and asthma (31).

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