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Another important site of histamine storage and release is the enterochromaffin-like (ECL) cell of the stomach. The most important pathophysiologic mechanism of mast cell and basophil histamine release is immunologic. These cells, if sensitized by IgE antibodies attached to their membranes, degranulate when exposed to the appropriate antigen.
Histamine is a weak base (a compound able to react with a hydrogen ion to form an acid) that can link with acid groups within the granules of the mast cells. [8] The mechanism of the displacement theory. The crux of this theory lies in the assumption that histamine liberators release histamine by displacing it from cells.
Histamine release is a common attribute of benzylisoquinolinium muscle relaxants. This problem generally decreases with increased potency and smaller doses. The need for larger doses increases the degree of this side-effect. Conformational or structural explanations for histamine release are not clear. [20]
Enterochromaffin-like cells or ECL cells are a type of neuroendocrine cell found in the gastric glands of the gastric mucosa beneath the epithelium, in particular in the vicinity of parietal cells, that aid in the production of gastric acid via the release of histamine. They are also considered a type of enteroendocrine cell. [1]
Histamine receptors are proteins that bind with histamine, a neurotransmitter involved in various physiological processes. There are four main types: H1, H2, H3, and H4. H1 receptors are linked to allergic responses, H2 to gastric acid regulation, H3 to neurotransmitter release modulation, and H4 to immune system function.
Degranulation in mast cells is part of an inflammatory response, and substances such as histamine are released. Granules from mast cells mediate processes such as "vasodilation, vascular homeostasis, innate and adaptive immune responses, angiogenesis, and venom detoxification."
A-fragments form distinct structural domains of approximately 76 amino acids, coded for by a single exon within the complement protein gene. The C3a, C4a and C5a components are referred to as anaphylatoxins: [4] [5] they cause smooth muscle contraction, vasodilation, histamine release from mast cells, and enhanced vascular permeability. [5]
They block mast cell degranulation, stabilizing the cell and thereby preventing the release of histamine and related mediators. One suspected pharmacodynamic mechanism is the blocking of IgE-regulated calcium channels. Without intracellular calcium, the histamine vesicles cannot fuse to the cell membrane and degranulate. [1]