Enigma of Disodium Cromoglycate Action on Mast Cells

Krüger, Per Gøran; Bloom, Gunnar D.

doi:10.1159/000232330

Cited by 9 publications

(4 citation statements)

References 8 publications

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“…The histamine release brought about by compound 48/80 at a concentration of 0.13 ¿ig/ml, which was used throughout the study, has been reported to be depressed by DSCG at concentrations of 2 X 10~4 M and 10~3M if added simultaneously with the liberator [Kruger and Bloom, 1979]. In that study, mixed cell suspensions from the peritoneal cavity of male rats of the Wistar strain were used.…”

Section: Discussionmentioning

confidence: 99%

“…In a previous report [Kruger and Bloom, 1979], the question was raised whether or not we may be overlooking certain indirect effects of the potent drug DSCG. In the light of Marcelle's [1970] findings that the bronchoconstrictive effect of histamine is not inhibited by phentolamine, but that this response is effectively reduced by DSCG, we suggest a reconsideration of the proposi tion by Cox [1976] that DSCG has no effect on adrenergic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, binding of labelled drug was transient and very weak. In rat mast cells, it has been reported that DSCG had no inhibitory effect on histamine release values if the cells were pre-incubated with the drug for 40 min prior to stimulation with antigen, compound 48/80 or ATP [Kruger and Bloom, 1979], Those authors also observed that if the drug was added simultaneously with antigen or a low dose of compound 48/80, a repression of histamine release occurred. No such effect was noted if ATP was employed as histamine libera tor.…”

Section: Introductionmentioning

confidence: 95%

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Anomalous Effects of Disodium Cromoglycate

Alm

Bloom

Henriksson

1981

Int Arch Allergy Immunol

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The effects of disodium cromoglycate (DSCG) on in vitro histamine release from peritoneal and pleural mast cells, and a possible interference with adrenergic mechanisms was studied. Parallel to this study, the effects of DSCG on the well-established adrenoceptor-mediated amylase release from parotid glands were investigated. It was found that DSCG in low concentrations potentiates histamine release from peritoneal mast cells. Furthermore, this potentiation is enhanced by α-adrenoeeptor blockade and diminished by β-adrenoceptor antagonists. Histamine release from pleural mast cells is affected inversely to peritoneal cells, that is, the secretion is inhibited by DSCG at a high concentration but not at a low one. The inhibition is unaffected by α-blockers but totally abolished by the β-antagonist propranolol. The amylase release induced by norepinephrine, mediated via β₁-adrenoceptors, is depressed by DSCG. The β-antagonist-sensitive amylase release induced by phentolamine is also inhibited by DSCG. Finally, DSCG alone induces amylase release from the parotid gland. These results would seem to indicate that DSCG exerts some α-adrenoceptor activity. However, it is not possible, at present, to state whether this activity is of agonistic nature. DSCG has effects which with respect to pattern, correspond well to the action of β-adrenoceptor agonists.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

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Anomalous Effects of Disodium Cromoglycate

Alm

Bloom

Henriksson

1981

Int Arch Allergy Immunol

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“…Prevention of mediator release from sensitized mast cells has been considered as the mechanism of action of disodium cromoglycate (DSCG), although recent evidence has been accumulated against this view [1][2][3]. However, a new interesting hypothesis concerning the protective action of DSCG against the contraction induced in smooth muscle by various pharmacological stimulants has recently been experimentally supported [4,5].…”

Section: Introductionmentioning

confidence: 99%

Further studies on the effects of disodium cromoglycate on guinea pig ileum

Arruzazabala¹,

Alvarez²

1982

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Transmural electrical stimulation was carried out on innervated strips of the longitudinal muscle of guinea pig ileum. Disodium cromoglycate (DSCG) inhibited the electrically induced contractions. Five minutes later, prostaglandin E2 (2.5 ng/ml) was added to the bath and it reversed the action of DSCG. Furthermore, DSCG inhibits significantly the guinea pig ileum contractions induced by nicotine and also those induced by histamine and acetylcholine on ileum denervated by cooling. These results suggest that DSCG effects on guinea pig ileum contraction are mediated by membrane-stabilizing properties of this drug on smooth muscle fibres as well as on myenteric plexus.

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Perspectives on the in vitro evaluation of anti‐anaphylactic agents

Weinryb¹,

Coutts²,

Khandwala³

1983

Drug Development Research

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Weinryb, I., S.M. Coutts, and A.S. Khandwala: Perspectives on the in vitro evaluation of anti-anaphylactic agents. Drug Dev. Res. 3213-219, 1983. In vitro models of anaphylaxis such as the release of mediators from the mast cell can do more than identify compounds with intrinsic anti-allergic activity; they have the potential for development of a detailed profile of activity that may be compared and contrasted in several ways to that of disodium cromoglycate. These parameters include effects upon a) immunologic versus nonimmunologic release, b) IgE-versus IgG-provoked release, c) timing of compound addition relative to challenge, d) repeated administration (presence or absence of tachyphylaxis), e) wash-out of agent (reversibility), and 9 other granulocyte models relative to the mast cell. Use of in vitro models of anaphylaxis in this way allows an early judgment to be made about the extent to which a new compound presents a novel anti-allergic profile.

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Enigma of Disodium Cromoglycate Action on Mast Cells

Cited by 9 publications

References 8 publications

Anomalous Effects of Disodium Cromoglycate

Anomalous Effects of Disodium Cromoglycate

Further studies on the effects of disodium cromoglycate on guinea pig ileum

Perspectives on the in vitro evaluation of anti‐anaphylactic agents

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