Inhibition of Antigen-Induced Histamine Release by β-Adrenergic Stimulants &lt;i&gt;in vivo&lt;/i&gt;

Fügner, A

doi:10.1159/000231810

Cited by 28 publications

(10 citation statements)

References 23 publications

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“…As to the mechanism of anti-allergic action of /J-agonists, it is widely accepted that /3-agonists inhibit the release of histamine and other mediators of ana phylaxis from mast cells via elevation of the cellular level of cAMP [2,28], This concept has been sup ported by in vitro [1][2][3][4][5][6][7][8][9] as well as in vivo [29] experi ments. Fiigner [29] demonstrated, using the method of passive peritoneal anaphylaxis in rats, that /3-agonists such as fenoterol, salbutamol and isoproterenol mark edly inhibited IgE-mediated histamine release and dye leakage into the peritoneal cavity.…”

Section: Discussionmentioning

confidence: 99%

“…Fiigner [29] demonstrated, using the method of passive peritoneal anaphylaxis in rats, that /3-agonists such as fenoterol, salbutamol and isoproterenol mark edly inhibited IgE-mediated histamine release and dye leakage into the peritoneal cavity. In the present work, too, isoproterenol inhibited the release of hista mine, but there was no definite correlation between inhibition of the vascular permeability and inhibition of the histamine release ( fig.…”

Section: Discussionmentioning

confidence: 99%

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Mechanism of Antianaphylactic Action of β-Agonists in Allergic Inflammation of Air Pouch Type in Rats

Ohuchi¹,

Hirasawa²,

Takeda³

et al. 1987

Int Arch Allergy Immunol

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Using an experimental model of allergic inflammation of air pouch type in rats, the mechanism of antiallergic action of β-agonists was examined. In this model an immediate increase in vascular permeability and histamine level in the pouch fluid was observed after injecting the antigen (azobenzene arsonate-conjugated acetyl bovine serum albumin) solution into the preformed air pouch on the back of the sensitized rats. The same type of reaction was inducible by injecting anti-rat IgE into the preformed air pouch, but not IgG2a. This fact indicates that the immediate increase in vascular permeability and histamine level is an IgE-mediated anaphylactic reaction. When β-agonists such as isoproterenol, procaterol and salbutamol were injected into the air pouch together with the antigen, the anaphylactic increase in vascular permeability was suppressed dose-dependently without concomitant decrease in histamine level in the pouch fluid. In contrast, disodium cromoglycate, an inhibitor of degranulation of mast cells, the anaphylactic vascular permeability increase was suppressed in parallel with a decrease of the histamine level. Propranolol, a β-antagonist, counteracted the effect of β-agonists. Serotonin-induced vascular permeability was also suppressed dose-dependently by treatment with β-agonists. Furthermore, vascular permeability in the postanaphylactic phase of the present experimental model was also suppressed by isoproterenol. These results indicate that β-agonists exert their antiallergic effect by inhibiting the reactivity of local vasculature to chemical mediators released from mast cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mechanism of Antianaphylactic Action of β-Agonists in Allergic Inflammation of Air Pouch Type in Rats

Ohuchi¹,

Hirasawa²,

Takeda³

et al. 1987

Int Arch Allergy Immunol

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“…This may be due to its intraperitoneal injection. DSCG [3] and WY-16.922 which is an orally effective anti allergic agent [13]; they have been demon strated to inhibit histamine release in similar experiments.…”

Section: Discussionmentioning

confidence: 99%

Anti-Allergic Activities of a New Benzopyranopyridine Derivative Y-12,141 in Rats

Goto¹,

Terasawa²,

Maruyama³

1979

Int Arch Allergy Immunol

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Passive cutaneous anaphylaxis (PCA) mediated in rats by IgE-like antibodies against egg albumin or the benzylpenicilloyl determinant was inhibited in a dose-dependent manner by intravenous treatment with Y-12,141; the ED50 was 0.09–0.2 mg/kg. The inhibitory effect of Y-12,141 on PCA was about 5 times as potent as that of disodium cromoglycate (DSCG). Oral treatment with Y-12,141 resulted in the inhibition of PCA, showing an ED₅₀ of 2.5 mg/kg. This action of Y-12,141 on PCA was considered to be due to the inhibition of the release of allergic mediators from mast cells in a manner similar to DSCG. The present results suggest that Y-12,141 may have an anti-allergic activity.

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“…The effect of /i-sympathicomimetic drugs in modifying the release of histamine has also been demonstrated in vivo in rats by means of the 'passive peritoneal anaphylax is' (PPA) model [7]. Finally, Lamkin et al [10] and Jorde and Schata [9] have shown that /i-adrenergic drugs inhibit the histamine response in human skin.…”

Section: Discussionmentioning

confidence: 99%

Immunological Release of Histamine from Human Lung

Morr¹

1979

Respiration

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Human lung tissue passively sensitized with anti-grass pollen IgE antibodies release histamine upon exposure to specific grass pollen antigen. Fenoterol, a β₂-sympathomimetic stimulator drug, is shown to be a potent inhibitor of antigen-induced release of histamine. This inhibitory effect occurred with fenoterol concentrations of 2 × 10^-8 to 1 × 10^-7M, and was determined by 67 and 95%, respectively. Thus, the β₂-receptor stimulator fenoterol is a valuable drug for treating allergic bronchial asthma since it exhibits a combination of prophylactic and direct therapeutic properties.

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Inhibition of Antigen-Induced Histamine Release by β-Adrenergic Stimulants <i>in vivo</i>

Cited by 28 publications

References 23 publications

Mechanism of Antianaphylactic Action of β-Agonists in Allergic Inflammation of Air Pouch Type in Rats

Mechanism of Antianaphylactic Action of β-Agonists in Allergic Inflammation of Air Pouch Type in Rats

Anti-Allergic Activities of a New Benzopyranopyridine Derivative Y-12,141 in Rats

Immunological Release of Histamine from Human Lung

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