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It has been known for more than one hundred years that an intravenous injection of histamine causes a fall in the blood pressure. [30] The underlying mechanism concerns both vascular hyperpermeability and vasodilation. Histamine binding to endothelial cells causes them to contract, thus increasing vascular leak.
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]
These endothelial products include nitric oxide and endothelin-1 that are released in response to either chemical stimuli, like histamine, or increased shear stress on the blood vessel (meaning the amount of stress exerted by blood on the blood vessel walls). While nitric oxide causes vasodilation, endothelin-1 causes vasoconstriction.
The extent of vasoconstriction may be slight or severe depending on the substance or circumstance. Many vasoconstrictors also cause pupil dilation. Medications that cause vasoconstriction include: antihistamines, decongestants, and stimulants. Severe vasoconstriction may result in symptoms of intermittent claudication. [1]
Endogenous substances and drugs that cause vasodilation are termed vasodilators. Many of these substances are neurotransmitters released by perivascular nerves of the autonomic nervous system [ 6 ] Baroreceptors sense blood pressure and allow adaptation via the mechanisms of vasoconstriction or vasodilation to maintain homeostasis .
Vasodilation and increased permeability of capillaries are a result of both H1 and H2 receptor types. [33] Stimulation of histamine activates a histamine (H2)-sensitive adenylate cyclase of oxyntic cells, and there is a rapid increase in cellular [cAMP] that is involved in activation of H+ transport and other associated changes of oxyntic cells ...
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."
Once released, the histamine can react with local or widespread tissues through histamine receptors. [citation needed] Histamine, acting on H 1-receptors, produces pruritus, vasodilation, hypotension, flushing, headache, bradycardia, bronchoconstriction, increase in vascular permeability and potentiation of pain. [2]