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Presynaptic modulation by adrenaline of 3H-noradrenaline release in rabbit ear artery

Abrahamsen, J.; Nedergaard, O.A.

Pharmacology 42(2): 79-85

1991


ISSN/ISBN: 0031-7012
PMID: 1648235
DOI: 10.1159/000138776
Accession: 041052874

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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 3H-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 3H overflow was determined. Adrenaline (10(-8) to 10(-6) mol/l) and clonidine (10(-9) to 10(-6) mol/l) reduced the stimulation-evoked 3H 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 3H 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 3H 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.

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