Adrenaline released as a cotransmitter does not enhance stimulation-evoked 3H-noradrenaline release from rabbit isolated aorta.

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 x 10(-6) M) or noradrenaline (10(-8)-3 x 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.