Anomalous effects of disodium cromoglycate. A study on two secretory systems.

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. Further more, this potentiation is enhanced by alpha-adrenoceptor blockade and diminished by beta-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 alpha-blockers but totally abolished by the beta-antagonist propranolol. The amylase release induced by norepinephrine, mediated via beta1-adrenoceptor, is depressed by DSCG. The beta-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 alpha-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 beta-adrenoceptor agonists.