Abstract
PGE 2, PGE 1, PGF 2α and PGD 2 dose dependently potentiated the ACh-evoked catecholamine (CA) release from perfused dog adrenal glands. These prostaglandins by themselves slightly stimulated CA release. PGE 2 potentiated the CA release induced by stimulation of nicotinic or muscarinic cholinergic receptors and also by stimulation with excess K + or caffeine. However, PGE 2 did not affect the release induced by caffeine. However, PGE 2 did not affect the release induced by caffeine in the absence of extracellular Ca 2+. ACh stimulated the 45Ca efflux from adrenals prelabelled with 45Ca. PGE 2 enhanced the ACh-stimulated 45Ca efflux. The CA release in response to ACh or nicotine was slightly but significantly reduced by pretreatment of the adrenals with indomethacin. SC19220, a specific prostaglandin antagonist significantly reduced the ACh-evoked CA release and blocked the enhancing action of PGE 2 on the stimulation-evoked CA release. The results showed that prostaglandins stimulated the CA release evoked in perfused dog adrenals and that the effect on the Ca 2+ flux across the plasma membrane could be involved in the prostaglandin mechanism of action. The possibility is suggested that prostaglandins formed endogenously in response to physiological stimulation of chromaffin cells could play a facilitating, modulatory role in CA release.
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