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

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1
Department of Pharmacology, School of Medicine, Odense University, Denmark.

Abstract

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.

PMID:
2566930
DOI:
10.1007/bf00173578
[Indexed for MEDLINE]

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