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

Summary

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 × 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 × 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 × 10⁻⁵ mol/l) plus corticosterone (4 × 10⁻⁵ mol/l), cocaine (3.3 × 10⁻⁶ mol/l) plus normetanephrine (4 × 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 > 3 > 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 α-adrenoceptor antagonists. Our results suggest that adrenaline activates inhibitory α₂-adrenoceptors, but not facilitatory β-adrenoceptors on postganglionic sympathetic nerve terminals in rabbit aorta.