Vasoactive amines are preformed mediators that influence vascular responses during inflammation.
Histamine storage and release
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Histamine is the major vasoactive amine. It is stored preformed in granules of mast cells, blood basophils, and platelets, allowing rapid release early in inflammation.
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Mast cells are the richest source of histamine and normally lie in connective tissue adjacent to blood vessels.
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Stimuli for mast cell degranulation and histamine release include IgE antibody binding, complement anaphylatoxins C3a and C5a, and physical injury from trauma, cold, or heat.
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Antibodies and complement products bind specific mast cell receptors and trigger signaling that induces rapid degranulation.
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Substance P and cytokines such as IL-1 and IL-8 may also trigger histamine release.
Histamine effects and receptor blockade
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Histamine dilates arterioles and increases venular permeability, acting mainly through H1 receptors on microvascular endothelial cells.
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Common antihistamine drugs used for inflammatory reactions such as allergies bind and block H1 receptors.
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Histamine contracts some smooth muscles, but leukotrienes are much more potent and relevant in bronchial smooth muscle spasm, such as in asthma.
Serotonin
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Serotonin, also called 5-hydroxytryptamine, is a preformed vasoactive mediator present in platelets and certain neuroendocrine cells, including those in the gastrointestinal tract.
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Serotonin is a vasoconstrictor, but its importance in inflammation is unclear.