Regulation of noradrenaline overflow in rat cerebral cortex by prostaglandin E2.
1 The effects of prostaglandin E2 (PGE2), PGF2 alpha and PGI2 and of inhibitors of prostaglandin synthesis and action, on the K+-evoked [3H]-noradrenaline ([3H]-NA) overflow from rat cerebral cortex slices have been investigated. 2 PGE2 reduced, while indomethacin (a prostaglandin synthesis inhibitor) or SC 19220 (a prostaglandin receptor antagonist) increased, the evoked overflow compared with controls. 3 The inhibition of [3H]-NA overflow by PGE2 was dose-dependently antagonized by SC 19220. 4 The results indicate that PGE2 modulates NA release in rat cerebral cortex in vitro.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D011464:Epoprostenol / Q000494:pharmacology; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011458:Prostaglandins E / Q000502:physiology*; D051381:Rats
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D011448:Prostaglandin Antagonists; D011458:Prostaglandins E; D011464:Epoprostenol; D011188:Potassium; D009638:Norepinephrine; D007213:Indomethacin