Role of adenosine 3?,5?-cyclic monophosphate in adrenoceptor-mediated control of 3H-noradrenaline secretion in guinea-pig ileum myenteric nerve terminals

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Abstract
Summary Secretion of 3H-noradrenaline was evoked by electrical field stimulation (1 Hz, 300 shocks) in guinea-pig ileum myenteric plexus. The role of cyclic nucleotides in the presynaptic receptor-mediated control of 3H-noradrenaline secretion was studied. The secretion of 3H-noradrenaline was maximally enhanced to the same extent, viz. 300–400% of control, by two analogues of cyclic AMP (8-Br cyclic AMP and dibutyryl cyclic AMP), by an adenylate cyclase activator (forskolin) and by three structurally different inhibitors of phosphodiesterase (3-isobutyl-1-methylxanthine, SQ 20,006 and Ro 20–1724), but not altered by two analogues of cyclic GMP (8-Br cyclic GMP and dibutyryl cyclic GMP). Added separately an α2-adrenoceptor antagonist (yohimbine) and a β-adrenoceptor agonist (isoprenaline) enhanced the 3H-noradrenaline secretion. Yohimbine, but not isoprenaline, increased additively the ‘maximal enhancement’ of the 3H-noradrenaline secretion caused by 3-isobutyl-1-methylxanthine. These results suggest that neuronal cyclic AMP may be involved in β-but not in α-adrenoceptor-mediated control of 3H-noradrenaline secretion in guinea-pig ileum myenteric nerve terminals.

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