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Stimulation‐evoked release of [ 3 H]‐noradrenaline by 1, 10 or 100 pulses and its modification through presynaptic α 2 ‐adrenoceptors
Author(s) -
Marshall Ian
Publication year - 1983
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.1476-5381.1983.tb09383.x
Subject(s) - yohimbine , stimulation , tritium , endocrinology , pulse (music) , prazosin , medicine , chemistry , antagonist , agonist , adrenergic , clonidine , phenylephrine , biology , receptor , blood pressure , physics , detector , nuclear physics , engineering , electrical engineering
1 Mice isolated vasa deferentia were loaded with 1‐[7, 8‐ 3 H]‐noradrenaline and subsequently field stimulated with 1, 10 or 100 pulses (2 ms pulse width, 1 Hz). The tritium overflow was separated into [ 3 H]‐noradrenaline and its 3 H‐metabolites. 2 The resting release of tritium contained about 7% [ 3 H]‐noradrenaline, 33% [ 3 H]‐3, 4‐dihydroxyphenylglycol ([ 3 H]‐DOPEG) and 60% 3 H‐non‐catechols with usually less than 1% [ 3 H]‐dihydroxymandelic acid ([ 3 H]‐DOMA). The proportion of the tritium as [ 3 H]‐noradrenaline increased with stimulation train length to 35% with 100 pulses; this increase in [ 3 H]‐noradrenaline was associated with falls in [ 3 H]‐DOPEG and 3 H‐non‐catechols. Generally the proportional increase in [ 3 H]‐noradrenaline on stimulation was about 10 × total tritium when compared with the resting release. 3 The fractional release of [ 3 H]‐noradrenaline per pulse was independent of train length, averaging about 6 × 10 −6 . This was reduced by the α 2 ‐adrenoceptor agonist clonidine (0.3–30 n m ) with an IC 5 o of 4.8 n m (10 pulses at 1 Hz). 4 The α 2 ‐adrenoceptor antagonist, yohimbine (10–100 n m ), did not alter the fractional release of [ 3 H]‐noradrenaline elicited by 1 pulse. The antagonist did not change the amount or composition of the resting or evoked tritium overflow. However, yohimbine (l‐100 n m ) increased the fractional release of [ 3 H]‐noradrenaline per pulse for trains of 10 or 100 pulses (1 Hz) in a concentration‐dependent fashion. An increase above controls was significant only with 100 pulses and yohimbine, 30 n m . 5 The results show that the release of noradrenaline during trains of pulses in the mouse vas deferens can be regulated through presynaptic α 2 ‐adrenoceptors. There was no evidence of inhibition by noradrenaline of its own release following a single pulse.