Receptors Mediating Some Actions of Histamine

Ash, A. S. F.; Schild, H. O.

doi:10.1111/j.1476-5381.1966.tb01674.x

Cited by 621 publications

(220 citation statements)

References 24 publications

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“…Histamine exerts a variety of rapid inflammatory effects including bronchoconstriction, vasodilation, increased vascular permeability and stimulation of afferent sensory nerve terminals [5]. These effects are mostly mediated by interaction with H 1 receptors [6]and they are responsible for the majority of acute symptoms in bronchial asthma, allergic rhinitis and urticaria [7]. However, histamine may also influence immune responses by modulating the activity of T cells [8], monocytes [9]and macrophages [10].…”

Section: Introductionmentioning

confidence: 99%

Histamine-Induced Activation of Human Lung Macrophages

Marone

Gentile²,

Petraroli³

et al. 2001

Int Arch Allergy Immunol

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Background: Histamine plays a central role in the pathogenesis of allergic and inflammatory diseases by modulating vascular and airway responses. Increasing evidence suggests that histamine also regulates the function of inflammatory and immune cells. Macrophages are primarily involved in inflammatory diseases of the lung. We explored the ability of low concentrations of histamine to induce the release of proinflammatory mediators from human lung macrophages. Methods: Macrophages purified (>95%) from lung parenchyma by Percoll density gradients and adherence to polystyrene dishes were incubated (37°C, 2–24 h) with histamine (10^–9–10^–6M). At the end of incubation, the release of β-glucuronidase and IL-6 was determined. Results: Histamine induced a concentration-dependent release of β-glucuronidase and IL-6 with a maximum release after 2 and 6 h of incubation, respectively. Exocytosis induced by histamine was noncytotoxic and was Ca²⁺- and temperature-dependent. The effect of histamine was inhibited by the H₁ receptor antagonist fexofenadine but not by the H₂ antagonist ranitidine. Conclusions: These data indicate that histamine is an effective stimulus for exocytosis and cytokine production from human lung macrophages. These effects are inhibited by pharmacological concentrations of fexofenadine. Our results suggest that histamine may contribute to the long-term evolution of lung inflammation and tissue remodelling in allergic diseases by modulating the production of proinflammatory and immunoregulatory mediators by macrophages.

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Section: Introductionmentioning

confidence: 99%

Histamine-Induced Activation of Human Lung Macrophages

Marone

Gentile²,

Petraroli³

et al. 2001

Int Arch Allergy Immunol

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“…Histamine has at least two kinds of effects (19 compounds (e.g., metiamide, burimamide, and betaimide) have been called H2 receptor actions (19,20,21).…”

Section: Resultsmentioning

confidence: 99%

Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability.

Brigham¹,

Bowers²,

Owen³

1976

J. Clin. Invest.

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A B S T R A C T To see whether antihistamines could prevent and reverse histamine-induced pulmonary edema and increased lung vascular permeability, we compared the effects of a 4-h intravenous infusion of 4 /Ag/kg per min histamine phosphate on pulmonary hemodynamics, lung lymph flow, lymph and plasma protein content, arterial blood gases, hematocrit, and lung water with the effects of an identical histamine infusion given during an infusion of diphenhydramine or metiamide on the same variables in unanesthetized sheep. Histamine caused lymph flow to increase from 6.0±0.5 to 27.0±5.5 (SEM) ml/h (P <0.05), lymph: plasma globulin concentration ratio to increase from 0.62±0.01 to 0.67±0.02 (P < 0.05), left atrial pressure to fall from 1+1 to -3±1 cm H20 (P < 0.05), and lung lymph clearance of eight protein fractions ranging from 36 to 96 A molecular radius to increase significantly. Histamine also caused increases in lung water, pulmonary vascular resistance, arterial Pco2, pH, and hematocrit, and decreases in cardiac output and arterial Po2. Diphenhydramine (3 mg/kg before histamine followed by 1.5 mg/ kg per h intravenous infusion) completely prevented the histamine effect on hematocrit, lung lymph flow, lymph protein clearance, and lung water content, and reduced histamine effects on arterial blood gases and pH. 6 mg/kg diphenhydramine given at the peak histamine response caused lymph flow and lymph: plasma protein concentration ratios to fall. Metiamide (10 mg/ Description of the preparation We used an unanesthetized, chronic sheep preparation described previously (1-4). Each animal was prepared by a series of three staged thoracotomies during which nonpulmonary contributions to a large lymph node in the posterior mediastinum (caudal mediastinal node) were resected;

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“…Histamine stimulates two types of receptors; HIreceptors (Ash & Schild 1966) and Ha-receptors (Black et al 1972). In the present study, the HI-receptor blocked with mepyramine.…”

mentioning

confidence: 95%

An inhibitory effect of histamine on the rat anococcygeus muscle

Oriowo

1982

Journal of Pharmacy and Pharmacology

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The rat anococcygeus muscle contracts in response to noradrenaline, 5-hydroxytryptamine (5-HT), acetylcholine and carbachol (Gillespie 1972). It is also contracted by high doses of histamine. However, the responses to histamine showed tachyphylaxis after a single dose. In a similar preparation in the cat (Gillespie & McGrath 1974) and the rabbit (Creed et a1 1977), histamine-induced contractions were abolished by mepyramine suggesting an action on histamine HIreceptors. It was also observed that metiamide, an H,-receptor antagonist (Black et a1 1973) potentiated histamine-induced contractions in the rabbit anococcygeus which might suggest the presence of histamine H,-receptors in this species. This communication, reports the inhibitory effect of histamine on the rat isolated anococcygeus muscle.Adult male rats (ca. 250 g) were killed by a blow on the head and then bled. The two anococcyeus muscles were removed according to Gillespie (1972) and suspended in a 20.0 ml organ bath containing aerated Tyrode solution (NaCI 137; KCI 2.7; CaCl, 1.8; MgCI, 0.9; NaH,PO, 0.3; NaHCO, 11.9 and glucose 5.6 mmol litre-') at 37 "C. Isotonic contractions (under a tension of 0.5 g) were recorded. Drugs used were: histamine acid phosphate; dimaprit; mepyramine maleate; impromidine; cimetidine; metiamide; acetylcholine chloride; carbachol ; ( -)-noradrenaline bitartrate and 5-hydroxytryptamine creatinine sulphate. All drug concentrations refer to the base.The muscle has no intrinsic tone, hence inhibitory effects of histamine and two selective H,-receptor agonists-dimaprit (Parsons et al 1977) and impromidine (Durant et a1 1978) were tested against agonistinduced contractions in the presence of mepyramine (1 p~) to block HI-receptors. In preliminary experiments when noradrenaline, carbachol and ACh were used as agonist, very high concentrations of histamine (> M) were needed to demonstrate an inhibitory effect. However, much lower doses (approx. 2 x M)

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Receptors Mediating Some Actions of Histamine

Cited by 621 publications

References 24 publications

Histamine-Induced Activation of Human Lung Macrophages

Histamine-Induced Activation of Human Lung Macrophages

Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability.

An inhibitory effect of histamine on the rat anococcygeus muscle

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