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Prejunctional α 2 ‐adrenoceptors in mouse atria function through G‐proteins which are sensitive to N‐ethylmaleimide, but not pertussis toxin
Author(s) -
Murphy Timothy V.,
Foucart Sylvain,
Majewski Henryk
Publication year - 1992
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.1476-5381.1992.tb14427.x
Subject(s) - pertussis toxin , idazoxan , endocrinology , medicine , stimulation , g protein , agonist , chemistry , alpha (finance) , receptor , biology , antagonist , prazosin , construct validity , nursing , patient satisfaction
1 The identity of the G‐proteins involved in prejunctional α 2 ‐adrenoceptor signal transduction in mouse atria was examined by use of the G‐protein inactivators N‐ethylmaleimide and pertussis toxin. 2 The α 2 ‐adrenoceptor partial agonist clonidine (0.03 μ m ) inhibited the electrical stimulation‐induced (S‐I) outflow of radioactivity from mouse atria which were incubated with [ 3 H]‐noradenaline and stimulated at 5 Hz. The partial α 2 ‐adrenoceptor agonist St 363 (10 μ m ) inhibited the S‐I outflow of radioactivity at the lower stimulation frequency of 2.5 Hz. The inhibitory effects of these compounds were not altered in mice pretreated with pertussis toxin (1.5 μg, i.v.). 3 The α 2 ‐adrenoceptor antagonist, idazoxan (0.1 μ m ), increased the S‐I outflow of radioactivity from mouse atria stimulated at 5 Hz, and this effect was not altered in atria from mice pretreated with pertussis toxin. 4 The inhibitory effects of clonidine and St 363 and the facilitatory effect of idazoxan on the S‐I outflow of radioactivity from mouse atria were significantly less in atria incubated with N‐ethylmaleimide (NEM, 3 μ m ) for 60 min before the [ 3 H]‐noradrenaline incubation. 5 The results suggest that prejunctional α 2 ‐adrenoceptors in mouse atria function through G‐proteins which are NEM‐sensitive, but pertussis toxin insensitive.