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pubmed:abstractText |
1 Guinea-pig vasa deferentia were continuously superfused after labelling the transmitter stores with [3H](-)-noradrenaline. Release of [3H]-(-)-noradrenaline was induced by transmural nerve stimulation. 2 Prostglandin E2 (14 nM) drastically reduced the release of [3H]-(-)-noradrenaline, while tetraethylammonium (2 mM), rubidium (6 mM), phenoxybenzamine (3 muM) each in the presence or absence of Uptake 1 or 2 blockade, and prolonged pulse duration (from 0.5 to 2.0 ms) all significantly increased the release of [3H]-(-)-noradrenaline per nerve impulse. 3 The inhibitory effect of prostaglandin E2 on evoked release of [3H]-(-)-noradrenaline was significantly reduced by tetraethylammonium, rubidium and prolonged pulse duration, whilst it was actually enhanced by phenoxybenzamine. This indicates that increased release of noradrenaline per nerve impulse does not per se counteract the inhibitory effect of prostaglandin E2. 4 It is concluded that tetraethylammonium, rubidium and prolonged pulse duration counteracted the inhibitory effect of prostaglandin E2 on T3H]-(-)-noradrenaline release by promoting calcium influx during the nerve action potential. The results are consistent with, and add more weight to the view that prostaglandins inhibit the release of noradrenaline by restriction of calcium availability.
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