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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.
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 histamine receptor H 2 belongs to the rhodopsin-like family of G protein-coupled receptors. It is an integral membrane protein and stimulates gastric acid secretion. It also regulates gastrointestinal motility and intestinal secretion and is thought to be involved in regulating cell growth and differentiation. [ 6 ]
The histamine receptors are a class of G protein–coupled receptors which bind histamine as their primary endogenous ligand. [1] [2] 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.
When activated, mast cells rapidly release characteristic granules, rich in histamine and heparin, along with various hormonal mediators and chemokines, or chemotactic cytokines into the environment. Histamine dilates blood vessels, causing the characteristic signs of inflammation, and recruits neutrophils and macrophages. [5]
Vasodilation works to decrease vascular resistance and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles. [17] When vasodilation causes systolic blood pressure to fall below 90 mmHg, circulatory shock is observed. [11]
Histamine H 1 receptors are activated by endogenous histamine, which is released by neurons that have their cell bodies in the tuberomammillary nucleus of the hypothalamus. The histaminergic neurons of the tuberomammillary nucleus become active during the 'wake' cycle, firing at approximately 2 Hz; during slow wave sleep , this firing rate ...
[6] [7] [8] VIP stimulates contractility in the heart, causes vasodilation, increases glycogenolysis, lowers arterial blood pressure and relaxes the smooth muscle of trachea, stomach and gallbladder. In humans, the vasoactive intestinal peptide is encoded by the VIP gene. [9] VIP has a half-life (t ½) in the blood of about two minutes. [10]