Studies on the release of histamine from isolated guinea pig mast cells stimulated by ionophore A23187 or by the anaphylactic reaction

Pearce, F. L.; Blum, Ulrike; Poblete-Freundt, G.; Schmutzler, W.

doi:10.1007/bf00517983

Cited by 17 publications

(5 citation statements)

References 21 publications

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“…Under the latter conditions, no influx of external cation is possible and the ob served inhibition cannot be explained by a direct effect on any simple calcium-gating mechanism. These results may also be com pared with our previous demonstration [9] that B u2 cA M P inhibited the release of his tamine from isolated guinea pig mesenteric mast cells treated with the ionophore A23187, conditions under which the calci um-gating mechanism was again bypassed. Cyclic AMP may then have a more general role in regulating the intracellular concen tration of calcium, whether derived from in ternal or external sources.…”

supporting

confidence: 78%

Effect of Cyclic AMP on Histamine Release Induced by Compound 48/80

Ennis¹,

Pearce²

1979

Int Arch Allergy Immunol

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Bu₂ cAMP(N⁶, O²′-dibutyryl adenosine-3′,5′-cyclic monophosphate) inhibited the response of rat peritoneal mast cells to compound 48/80 in the presence of calcium ions. In the absence of calcium, the nucleotide partially prevented the desensitization induced by chelating agents. The response of cells, allowed to accumulate Bu₂ cAMP in the presence of calcium (to avoid depletion of intracellular stores of the ion) and then challenged in the absence of extracellular calcium, was also inhibited. These results are discussed in terms of the postulated effects of Bu₂ cAMP on the calcium-gating mechanism operative in histamine secretion.

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supporting

confidence: 78%

Effect of Cyclic AMP on Histamine Release Induced by Compound 48/80

Ennis¹,

Pearce²

1979

Int Arch Allergy Immunol

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“…FIGURE 8 in the medium induces release of histamine from tissue mast cells (Cochrane and Douglas, 1974;Diamant and Patkar, 1975;Pearce et al, 1978). In the present study, histamine released from tissue stores in turn stimulated histamine H 2 receptors on myocardial cells, and thereby activated myocardial adenylate cyclase and increased tissue cyclic AMP levels (Verma and McNeill, 1976;Watanabe and Besch, 1974).…”

Section: U R a T I O N O F A 2 3 1 8 7 P E R F U S I O N ( S E C O supporting

confidence: 53%

Indirect and direct effects of the divalent cation ionophore A23187 on guinea pig and rat ventricular myocardium.

Lindemann¹,

Besch²,

Watanabe³

1979

Circulation Research

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SUMMARY The contractile and biochemical effects of the divalent cation ionophore A23187 were studied in isolated perfused guinea pig and rat ventricles. A23187 increased both cyclic adenosine 3':5'-monophosphate (cyclic AMP) and cyclic guanosine 3':5'-monophosphate (cyclic GMP) concentrations in guinea pig ventricles. Associated with these changes in nucleotide content were positive inotropic effects and activation of giycogen phosphorylase. Pretreatment of «nirrmln with reserpine to deplete endogenous catecholamine stores or pretreatment of hearts with propranolol failed to alter these ionophore-induced change*. In contrast, blockade of histamine (Hi) receptors with metiamide completely abolished the positive inotropic effects and activation of giycogen phosphorylase induced by A23187. In these metiamide-treated hearts, the ionophore-induced increase in cyclic AMP concentration was significantly attenuated, whereas the increase in cyclic GMP content persisted. A23187 produced a negative inotropic effect in hearts taken from rats treated with reserpine. In these rat hearts, cyclic AMP levels and giycogen phosphorylase activity were unchanged, whereas cyclic GMP concentrations were markedly increased. These results indicate that A23187 produces both indirect and direct effects on guinea pig ventricles. The indirect effects are mediated primarily by histamine, presumably released from tissue mast cells by the ionophore. Histamine in turn increases cyclic AMP levels, which leads to activation of phosphorylase and positive inotropic effects. The direct biochemical effect of A23187 is an increase in cyclic GMP concentrations. Ore Rea 44: [473][474][475][476][477][478][479][480][481][482] 1979

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“…A23187 secretory effects appear to be insensitive to regulatory systems and what was found in neutrophils is confirmed by experiments performed in other cell types characterized by an exocytotic secretory process. In guinea-pig mast cells, isoprenaline and adrenaline were effective inhibitors of anaphylactic histamine release, but they did not affect the secretory action of A23187 [44].…”

Section: Discussionmentioning

confidence: 93%