Adrenaline released as a cotransmitter does not enhance stimulation-evoked3H-noradrenaline release from rabbit isolated aorta

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Abstract
1 The aim of the present investigation was to examine if adrenaline released as a cotransmitter by field stimulation of sympathetic neurons in rabbit isolated aorta facilitates noradrenaline release by activation of presynaptic .beta.-adrenoreceptors. 2 Rabbit aortic rings were preincubated with adrenaline (10-8-3 .times. 10-6 M) or noradrenaline (10-8-3 .times. 10-6 M) prior to incubation with 3H-noradrenaline (3H-NA; 10-7 M). Subsequently, the tissues were subjected to repeated electrical-field stimulation. 3 Preincubation of aorta with either adrenaline or noradrenaline did not change the time course of repeated stimulation-evoked 3H-overflow from tissues preloaded with 3H-NA. 4 Propranolol (10-8-10-6 M) did not alter the stimulation-evoked 3H-overflow. 5 Rauwolscine (10-7-10-5 M) enhanced markedly the 3H-overflow, evoked by stimulation. In the presence of rauwolscine, propranolol (10-8-10-6 M) and metoprolol (10-8-10-6 M) did not change the 3H-overflow. 6 In experiments using rings of aorta exposed to adrenaline (10-8 M) for 30 min in the absence of cocaine, stimulation-evoked 3H-overflow was not affected after withdrawal of adrenaline. This was also the case in the presence of propranolol (10-6 M). 7 We conclude that adrenaline released as a cotransmitter from sympathetic nerve terminals in rabbit aorta does not facilitate noradrenaline release.

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