Histamine is what type of hormone

AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus. Author guidelines Reasons to publish Ethical policy Open-access policy Publication charges Author resource centre. Advanced Search Help.

The role of histamine in the neuroendocrine regulation of pituitary hormone secretion in European Journal of Endocrinology. Restricted access. In addition, few studies have tried to distinguish possible effects on presynaptic receptors, postsynaptic receptors, hypothalamic blood vessels or the hypophyseal portal blood vessels.

It is concluded that although there is good evidence now linking histamine and the hypothalamus more specific studies are required, for instance using microinjection or in vitro techniques and the more specific chemical tools now available, to enable a clearer understanding of the physiological role of histamine in the hypothalamus. The histamine receptor on parietal cells is the H2 type, and blocking the binding of histamine to this receptor is a widely used method for suppressing gastric acid secretion.

Smooth muscle around bronchi in the lungs and within the intestinal tract respond to histmine stimulation by contraction, although the magnitude of response varies considerably among species. These effects also depend on which receptor is being bound by histamine; for example, the H2 receptor mediates bronchodilation.

One of the first bioassays for histamine involved measuring contraction of guinea pig intestinal muscle. These effects on smooth muscle are manifest in a number of allergic reactions, for example, bronchocontriction in response to inhaled allergens. Histamine acts as a neurotransmitter within the central nervous system. The histaminergic neurons that secrete histmine are localized in small regions of the hypothalamus, but those neurons send axons widely throughout the brain.

Histamine appears to modulate a number of important processes in the brain, including wakefulness, cognitive ability and food consumption. Its activation is involved in the regulation of gastric acid secretion, gastrointestinal motility, and cell growth and differentiation. It is also suggested to have an immune-suppressive affect via inhibition of white blood cell chemotaxis i.

The H 3 receptor has a significant presence on CNS histaminergic neurons, eosinophils, dendritic cells and monocytes. It regulates the secretion of neurotransmitters, nerve supply to the heart and blood vessels and smooth muscle contraction. Lastly, the H4 receptor is mainly expressed on haematopoietic cells, as well as on various immune cells i.

Its activation thought to be involved in inflammation and allergic processes. Non-immunological histamine release involves the degranulation of stored histamine from mast cells and basophils or the passive transport of histamine in non-storing cells, which can be induced by endogenous neuropeptides, cytokines, complement or exogenous alcohol, food, medication factors.

In humans this involves two primary pathways: histamine N-methyltransferase HNMT catalysed-methylation of the imidazole ring and deamination of the main amino group involving diamine oxidase DAO. The end-result of both pathways are compounds that have limited histamine-receptor binding capacities. Histamine inactivated by this pathway is derived from cellular synthesis or transported from the extracellular space, whereupon it is converted to N-tele-methylhistamine with the addition of a methyl group from S-adenosyl-L-methionine and then to M-methylimidazole acetic acid before leaving the body via the urine.

Because this pathway inactivates exogenous histamine, DAO is largely expressed and released following a stimulus by intestinal epithelial cells, with a smaller presence in kidney and placental tissues. The intestinal absorption of histamine is largely inhibited by DAO, while any histamine that is absorbed is deaminated removal of an amine group to imidazole acetaldehyde, ammonia and hydrogen peroxide by the intestinal epithelial cells.

Histamine intolerance is the consequence of excess levels of endogenous histamine inducing a broad range of systemic physiological effects in the body. This is due in part to the range of organs and tissues that express histamine receptors, with symptoms of histamine intolerance presenting in gastrointestinal diarrhoea, abdominal pain, cramps, bloating, reflux , respiratory sneezing, rhinorrhoea, nasal congestion or swelling, phlegm, cough, asthma , cardiovascular arrhythmias, tachycardia, palpitations , integumentary urticarial, pruritis, flushing , CNS headache, dizziness, anxiety, sleep disturbances and reproductive tissues or organs dysmenorrhoea, menstrual headache.

These endogenous processes include impaired DAO or HNMT enzyme activity which can be genetic or acquired , excess histamine synthesis due to, mastocytosis, allergies or gastrointestinal issues damaged intestinal enterocytes, GIT bleeding, dysbiosis. Exogenous factors that may contribute to histamine intolerance relate to particular foods, medications and stress. Foods relevant to histamine intolerance include those that: contain high levels of histamine fermented foods such as sauerkraut, processed meat, dried anchovies, fish sauce, spinach, tomatoes, cocoa, eggplant, fish, chicken, yoghurt, soy, red wine ; induce histamine release from mast cells citrus foods, pineapple, bananas, strawberries, papaya, tomatoes, additives ; or other biogenic amines that may interfere with the binding of histamine to mucosal mucine resulting in more histamine in circulation.

Histamine-associated mechanisms associated with medication include inhibition of DAO activity muscle relaxants, narcotics, analgesics, local anaesthetics, antihypnotics, antihypertensives, antiarrhythmics, diuretics, antibiotics, antiemetics, bronchodilators, antiseptics, mucolytics, H2-receptor antagonists, antidepressants ; stimulation of histamine release painkillers, antibiotics, anti-hypotensives, anti-hypertensives, antitussives, cytostatics, diuretics, local anaesthetics, muscle relaxants, narcotics or inactivation of vitamin B6 antihypertensives, antibiotics, hormonal contraceptives.

Stress can also play a role due to the activation of mast cells by stress-induced hormones. The impact of chronic stress on the integrity of the intestinal epithelial lining, adversely influencing the histamine-inactivating capacity of intestinal DAO, is another process potentially contributing to increased levels of circulating histamine.

The complexity of histamine intolerance extends to the interaction between histamine, oestrogen and progesterone in the female body. Mast cells are a key factor underlying these interactions, with the presence of both oestrogen and progesterone receptors on mast cells and mechanistic evidence in vitro and in vivo suggesting a regulatory role of these steroid hormones on mast cell functionality and activity.

The binding of oestrogen to mast cell receptors stimulates the expression of H 2 and H 3 receptors, and induces rapid histamine degranulation, synthesis and release. Histamine, within female reproductive tissue, is derived from uterine- and ovarian epithelial and mast cells, and endometrial and myometrial endothelial cells. The degranulation and activity of histamine appears to fluctuate with menstrual hormonal secretions.

During a healthy menstrual cycle, there is a characteristic hormonal pattern involving luteinising hormone LH , follicle stimulating hormone FSH , oestrogen and progesterone. Animal data has demonstrated that cellular histamine concentrations in ovarian and uterine mast cells varies across the menstrual cycle, and the activation of mast cells within endometrial tissue is most significant during the premenstrual phase following the decrease in progesterone and oestradiol. A correlation between urinary histamine metabolites and plasma oestrogen levels in premenopausal women has been observed, as has significant associations between elevated midcycle serum oestradiol levels and skin prick test reactivity to histamine.