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Abstract
The effect of phorbol 12-myristate, 13-acetate (PMA), an activator of protein kinase C, on noradrenaline (NA) release from cat cerebral arteries preincubated with [ 3H]NA was investigated in order to examine the role of that enzyme in this secretion. PMA (3 μM) potentiated tritium release elicited by electrical stimulation (2 Hz, 0.3 ms) without modification of spontaneous secretion, whereas 4α-phorbol 12,13 didecanoate (3 μM), an inactive compound, had no effect. Tritium release evoked by tyramine was not modified by PMA. The electrically evoked tritium secretion was reduced by clonidine (1 μM) or B-HT 920 (0.1 μM), α 2-adrenoceptor agonists, and unaffected by yohimbine (1 μM), an α 2-adrenoceptor antagonist. The presence of clonidine, B-HT 920 or yohimbine reduced the action of PMA. The facilitatory effect of PMA was not increased by the Ca 2+ ionophore A23187 (5 μM). These results suggest that: (1) protein kinase C of perivascular adrenergic nerve endings participates in the exocytotic release of NA; (2) the effects of PMA could be partially due to an interference with prejunctional autoinhibitory α 2-adrenoceptors, and (3) the increase of intracellular Ca 2+ produced by A23187 appears to be inadequate for potentiating the action of PMA.
Published Version
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