Anomalous Effects of Disodium Cromoglycate

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Abstract
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.