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Sustained prejunctional facilitation of noradrenergic neurotransmission by adrenaline as a co‐transmitter in the portal vein of freely moving rats
Author(s) -
Coppes R.P.,
Brouwer F.,
Freie I.,
Smit J.,
Zaagsma J.
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb16992.x
Subject(s) - endocrinology , medicine , catecholamine , stimulation , neurotransmission , norepinephrine , epinephrine , chemistry , adrenergic , antagonist , anesthesia , receptor , dopamine
1 The duration of the facilitatory effect of adrenaline on the electrically evoked overflow of noradrenaline was studied in the portal vein of permanently adreno‐demedullated freely moving rats. 2 Rats were infused with adrenaline (20 or 100 ng min ‐1 ) for 2h. After an interval of 1 h, when plasma adrenaline had returned to undetectable levels, electrical stimulation resulted in an enhanced catecholamine overflow amounting to 219% (noradrenaline) and 241% (noradrenaline plus adrenaline) of control (saline infusion), respectively. 3 When stimulation was applied again, in the same animal, at 24, 48 and 72 h after the first stimulation episode, the evoked noradrenaline overflow was 150, 111 and 102% (after 20 ng ml ‐1 adrenaline) and 158, 134 and 105% (after 100 ng min ‐1 adrenaline) of control. 4 The β 2 ‐adrenoceptor antagonist, ICI 118,551 (0.3 mg kg ‐1 ), blocked the facilitatory effect obtained after the 100 ng min ‐1 adrenaline infusion on all days. 5 The results show that adrenaline, after being taken up by and released from sympathetic nerve terminals, is able to facilitate the evoked noradrenaline overflow through activation of prejunctional β 2 ‐adrenoceptors for at least 48 h after administration.