β‐Adrenoceptor mediated facilitation of noradrenaline and adenosine 5′‐triphosphate release from sympathetic nerves supplying the rat tail artery

The effects of prejunctional β‐adrenoceptor activation on electrically evoked noradrenaline (NA) and adenosine 5′‐triphosphate (ATP) were studied by use of continuous amperometry and conventional intracellular recording techniques. Excitatory junction potentials (e.j.ps) were used as a measure of ATP release, and NA‐induced slow depolarizations and oxidation currents as measures of NA release, from postganglionic sympathetic nerves innervating the rat tail artery in vitro. Isoprenaline (0.1 μm) increased the amplitude of e.j.ps, slow depolarizations and oxidation currents evoked by short trains of stimuli at 1 to 4 Hz. The facilitatory effect of isoprenaline on e.j.ps and oxidation currents was most pronounced on responses evoked by the first stimulus in a train. Isoprenaline (0.1 μm) did not detectably alter the amplitude‐frequency distribution of spontaneous e.j.ps. The facilitatory effect of isoprenaline on e.j.ps, slow depolarizations and oxidation currents was abolished by the β‐adrenoceptor antagonist, propranolol (0.1 μm). Propranolol alone had no effect on e.j.ps, slow depolarizations or oxidation currents. Thus, activation of prejunctional β‐adrenoceptors increases the release of both NA and ATP from postganglionic sympathetic nerves. The findings are consistent with the hypothesis that NA and ATP are released from the same population of nerve terminals and presumably from the same vesicles. British Journal of Pharmacology (1997) 120, 769–776; doi:10.1038/sj.bjp.0700959