Presynaptic action of adrenaline on adrenoceptors modulating stimulation-evoked 3H-noradrenaline release from rabbit isolated aorta.

The purpose of this investigation was to study the effect of adrenaline on presynaptic adrenoceptors by recording the release of 3H-noradrenaline evoked by electrical-field stimulation. Adrenaline (10(-10)-3 x 10(-9) mol/l) had no effect on the 3H-overflow evoked by stimulation of aorta preloaded with 3H-noradrenaline. At 10(-8) and 3 x 10(-8) mol/l, the 3H-overflow was decreased by up to 47%. The maximum decrease was more marked in the presence of either cocaine (3 x 10(-5) mol/l) plus corticosterone (4 x 10(-5) mol/l), cocaine (3.3 x 10(-6) mol/l) plus normetanephrine (4 x 10(-5) mol/l), or desipramine (10(-6) mol/l) plus normetanephrine (10(-5) mol/l). The relationship between adrenaline-induced decrease and stimulation-frequency was dependent on the experimental design: either the decrease was the same at all frequencies (1-16 Hz) or it was more marked, the lower the frequency (1 greater than 3 greater than 8 Hz). Phentolamine and rauwolscine (both 10(-6) mol/l) antagonized the inhibitory effect of adrenaline (10(-8)-10(-6) mol/l). Phenoxybenzamine (10(-6) mol/l), prevented the inhibitory effect. No enhancing effect of adrenaline (10(-9)-10(-6) mol/l) was observed in the presence of these three alpha-adrenoceptor antagonists. Our results suggest that adrenaline activates inhibitory alpha 2-adrenoceptors, but not facilitatory beta-adrenoceptors on postganglionic sympathetic nerve terminals in rabbit aorta.