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Do mast cell degranulators release prostaglandins from frog atria?
European Journal of Pharmacology
|May 21, 1982
Summary
Compound 48/80 and d-tubocurarine stimulate frog atria via a common indirect pathway. Prostaglandin involvement is suggested, as indomethacin blocked these stimulant effects.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Histamine Research
Background:
- Isolated frog atria are sensitive to various stimuli.
- Mast cell degranulators can elicit physiological responses.
- Histamine, serotonin, and adrenergic pathways are involved in cardiac function.
Purpose of the Study:
- To investigate the mechanism of action of compound 48/80 and d-tubocurarine on frog atria.
- To explore the potential involvement of prostaglandins in these responses.
Main Methods:
- Isolated frog atria were treated with compound 48/80 and d-tubocurarine.
- Receptor blockers for H2-histamine, serotonin, and beta-adrenergic receptors were used.
- Experiments were conducted with indomethacin-treated atria (ex vivo and in vitro).
Main Results:
- Compound 48/80 and d-tubocurarine induced a delayed stimulation with tachyphylaxis and cross-tachyphylaxis.
- Blockade of H2-histamine, serotonin, and beta-adrenergic receptors did not inhibit the responses.
- Indomethacin treatment abolished the stimulant effects of mast cell degranulators.
Conclusions:
- A common indirect mechanism underlies the stimulatory effects of compound 48/80 and d-tubocurarine on frog atria.
- Prostaglandins likely play a role in mediating these responses.
- Further research is needed to elucidate the precise prostaglandin pathway involved.