Abstract
1 The release of radioactivity from rat isolated atria preloaded with [3H]-noradrenaline ([3H]-NA) evoked by electrical field stimulation (2Hz, 1 ms, 60s) of intraneuronal sympathetic nerves, high potassium (64.7 mm) or tyramine (0.3μm) was used as an index of noradrenaline release. 2 Activation of protein kinase C by phorbol 12-myristate 13-acetate (PMA) produced a concentration-dependent enhancement of field stimulation-induced outflow of radioactivity, whereas polymyxin B, an inhibitor of protein kinase C, reduced [3H]-NA release evoked by field stimulation. The enhancement observed in the presence of PMA was attenuated by polymyxin B (10 and 70 μm). 3 Release of noradrenaline evoked by membrane depolarization in a high potassium medium was similarly affected by PMA and polymyxin B. 4 In contrast, the release of noradrenaline evoked by the indirectly acting sympathomimetic amine, tyramine, was not altered by PMA. Polymyxin B in a concentration of 70 μm, but not 10 μm caused a slight reduction in tyramine-induced outflow of radioactivity. 5 The spontaneous outflow of radioactive compounds was not affected by either PMA or polymyxin B in the bathing medium. 6 The findings suggest that protein kinase C may play a role in the exocytotic release of noradrenaline but not in the displacement of noradrenaline by indirectly acting sympathomimetic amines.

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