Vasodilation histamine causing

Endogenous histamine has a modulating role in a variety of inflammatory and immune responses. Upon injury to a tissue, released histamine causes local vasodilation and leakage of plasma-containing mediators of acute inflammation (complement, C-reactive protein) and antibodies. Histamine has an active chemotactic attraction for inflammatory cells (neutrophils, eosinophils, basophils, monocytes, and lymphocytes). Histamine inhibits the release of lysosome contents and several T- and B-lymphocyte functions. Most of these actions are mediated by H2 or H4 receptors. Release of peptides from nerves in response to inflammation is also probably modulated by histamine, in this case acting through presynaptic H3 receptors. 

In humans, injection or infusion of histamine causes a decrease in systolic and diastolic blood pressure and an increase in heart rate. The blood pressure changes are caused by the direct vasodilator action of histamine on arterioles and precapillary sphincters the increase in heart rate involves both stimulatory actions of histamine on the heart and a reflex tachycardia. Flushing, a sense of warmth, and headache may also occur during histamine administration, consistent with the vasodilation. Vasodilation elicited by small doses of histamine is caused by H -receptor activation and is mediated primarily by release of nitric oxide from the endothelium (see Chapter 19). The decrease in blood pressure is usually accompanied by a reflex tachycardia. Higher doses of histamine activate the H2-mediated cAMP process of vasodilation and direct cardiac stimulation. In humans, the cardiovascular effects of small doses of histamine can usually be antagonized by Hi-receptor antagonists alone. 

As noted, mast cells and their mediators are integral components of the allergic response. Histamine, the main mediator involved in type I allergic reactions, is released from mast cells and basophils. Histamine is synthesized and stored in nearly all tissues, with especially high concentrations in the lungs, skin, stomach, duodenum, and nasal mucosa. Histamine causes smooth muscle contraction, increased vascular permeability, vasodilation,... 

Histamine causes vasodilation and bronchoconstriction. In the stomach, it stimulates the secretion of HC1. 

Bradykinin is a potent vasodilator that causes contraction of nonvascular smooth muscle, increases vascular permeability and it is also involved in the mechanism of pain. It has similar actions to histamine, and, like histamine, it is released from venules rather than arterioles. Bradykinin stimulates nitric oxide (NO) production by vascular endothelium. Histamine, released from mast cells in response to injury, inflammation or allergic responses, causes arteriolar vasodilatation, venous constriction in some vascular beds, and increased capillary permeability. 

The vasoconstrictive property of corticoids may contribute to their anti-inflammatory effects. The mechanisms by which topical corticoids cause vasoconstriction remains unclear but is thought to be related to their inhibition of natural vasodilators, histamine, bradykinins, and prostaglandins [2, 46]. Some have suggested that corticosteroids potentiate norepinephrine [34], while others suggest that corticoids cause the release of norepinephrine [81]. Corticoids are thought to also have a direct effect on vascular endothelial cells. 

Nerve receptors, or nociceptors, may release substance P, a peptide that causes vasodilation when released.20 This dilation occurs mainly through substance P-induced production of the vasodilator nitric oxide. Substance P also generates the release of histamine, leading to bradykinin release and activation of an inflammatory process. Capsaicin relieves pain by stimulating the release of substance P from sensory nerve fibers, which ultimately depletes stores of substance P. 

The group C counterirritants methyl nicotinate and histamine dihydrochloride produce vasodilation.24 Methyl nicotinate is a nicotinic acid derivative that produces prostaglandin-mediated vasodilation.46 NSAIDs and aspirin block the production of prostaglandins and decrease methyl nicotinate-induced vasodilation. Application over a large area has been reported to cause systemic symptoms and syncope, possibly due to vasodilation and a decrease in blood pressure.47 Patients should be educated to apply only scant amounts to the affected area to avoid this effect. 

An immediate reaction occurs within seconds to minutes, resulting in the rapid release of preformed mediators and newly generated mediators from the arachidonic acid cascade. Mediators of immediate hypersensitivity include histamine, leukotrienes, prostaglandin, tryptase, and kinins. These mediators cause vasodilation, increased vascular permeability, and production of nasal secretions. Histamine produces rhinorrhea, itching, sneezing, and nasal obstruction. 

C. The vasodilation produced by drug Y is antagonized by timolol, a (3-receptor antagonist. Although bradykinin, histamine, acetylcholine, and isoproterenol will all cause vasodilation, only isoproterenol does so by activating p-receptors. Phenylephrine is a sympathomimetic that is selec-... 

C. The vasodilation caused by bradykinin, histamine, hydralazine, and acetylcholine depends in part upon nitric oxide release from the endothelium. Minoxidil activates K+ channels, which results in vascular smooth muscle hyperpolarization and thereby relaxation. 

A slow intravenous injection of histamine produces marked vasodilation of the arterioles, capillaries, and venules. This causes a fall in blood pressure whose magnitude depends on the concentration of histamine injected, the degree of baroreceptor reflex compensation, and the extent of histamine-induced release of adrenal catecholamines. Vasodilation of cutaneous blood vessels reddens the skin of the face, while a throbbing headache can result from vasodilation of brain arterioles. Vasodilation is mediated through both Hj- and Hj-receptors on vascular smooth muscle. Stimulation of Hj-receptors produces a rapid and short-lived response, whereas stimulation of H2-receptors produces a more sustained response that is slower in onset. Stimulation of Hj-receptors on sympathetic nerve terminals inhibits the release of norepinephrine and its associated vasoconstriction. 

Have potent direct vasodilator actions on vascular smooth muscle Enhance gastric acid secretion through a histamine-like effect Cause hypotension and bradycardia... 

The stimulation of C fibers by capsaicin causes a subset of sensory airway neurons to release several neuropeptides, which include tachykinin, substance P and neurokinin A. In addition to capsaicin, other endogenous mediators including histamine, prostaglandins and bradykinins can also result in their release. These neuropeptides are responsible for neurogenic inflammation, which is characterized by vasodilation, mucus secretion, plasma protein extravasation, increased expression of the adhesion molecules and bronchoconstriction. 

A number of vasodilators, such as acetylcholine, bradykinin, adenine nucleosides, thrombin, histamine, and serotonin, require an intact vascular endothelium to exert their effects. For example, stimulation of endothelial cholinergic receptors causes the release of endothelium-derived relaxing... 

Morphine releases histamine and may cause peripheral vasodilation and orthostatic hypotension (Figure 47.7). The cutaneous blood vessels dilate around the blush areas such as the face, neck, and upper thorax. Morphine causes cerebral vasodilation (due to increased carbon dioxide retention secondary to respiratory depression), and hence, it increases the cerebrospinal fluid pressure. Therefore, morphine should be used cautiously in patients with either meningitis or a recent head injury. When given subcutaneously, morphine is absorbed poorly whenever there is either traumatic or hemorrhagic shock. 

Histamine receptors variously mediate the bronchoconstrictant, inflammatory, irritant, vasodilator, gastric pepsin secretion and immune suppression actions of histamine. Associated with the immune response, cytokines cause release of histamine from mast cells. Histamine acts via HI, H2, H3 and H4 GPCRs. HI and H2 receptors couple via both Gas (elevating cAMP) and Gaq (elevating Ca2+ in a pertussis toxin-insensitive fashion) and H3 couples via Gai (decreasing cAMP). 

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