PRESYNAPTIC MODULATION BY ADRENALINE OF H-3 NORADRENALINE RELEASE IN RABBIT EAR ARTERY

The aim of the present investigation was to examine the ability of adrenaline to modulate presynaptically the stimulation-evoked release of noradrenaline from postganglionic sympathetic nerves in the rabbit ear artery. Strips of rabbit central ear artery were incubated with H-3-noradrenaline. Subsequently, they were washed repeatedly with physiological salt solution containing cocaine and corticosterone. The strips were subjected to repeated electrical-field stimulation (S1-S8, 150 pulses, 0.5 ms, 225 mA, 3 Hz) and the resultant H-3 overflow was determined. Adrenaline (10(-8) to 10(-6) mol/l) and clonidine (10(-9) to 10(-6) mol/l) reduced the stimulation-evoked H-3 overflow. Rauwolscine (10(-7) to 10(-5) mol/l) and phentolamine (3 x 10(-7) to 3 x 10(-5) mol/l) enhanced markedly the stimulation-evoked H-3 overflow. Rauwolscine (10(-6) mol/l) abolished the inhibitory effect of low concentrations of adrenaline (10(-8) to 10(-7) mol/l) and clonidine (10(-9) to 10(-7) mol/l) and attenuated the inhibitory effect of the highest concentration (10(-6) mol/l) of clonidine, but not that of adrenaline. In some experiments, the stimulation current was reduced to 175 mA in order to obtain similar reference release (S3) values despite the presence of rauwolscine. Even then, only the highest concentration (10(-6) mol/l) of adrenaline decreased the stimulation-evoked H-3 overflow. Facilitation was not seen. It is concluded that adrenaline activates inhibitory presynaptic alpha-2-adrenoceptors. Furthermore, adrenaline does not reveal the presence of presynaptic facilitatory beta-adrenoceptors in the rabbit ear artery.