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β‐Adrenoceptor stimulation enhances transmitter output from the rat phrenic nerve
Author(s) -
Wessler Ignaz,
Anschütz Stephanie
Publication year - 1988
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.1476-5381.1988.tb11574.x
Subject(s) - isoprenaline , stimulation , atenolol , endocrinology , medicine , propranolol , phrenic nerve , acetylcholine , neuromuscular transmission , chemistry , neuromuscular junction , biology , neuroscience , respiratory system , blood pressure
1 Neurally‐evoked output of newly synthesized [ 3 H]‐acetylcholine from the rat phrenic nerve was measured in the absence of cholinesterase inhibitors. 2 Noradrenaline and isoprenaline enhanced neurally‐evoked transmitter output markedly. Moreover, immediately after the application of noradrenaline the basal tritium efflux increased significantly. 3 Pretreatment with propranolol (0.1 μmol l −1 ) or atenolol (0.3 μmol l −1 ) completely prevented the stimulatory effect of noradrenaline and isoprenaline on evoked transmitter output. 4 The facilitatory effect of isoprenaline declined, when the exposure time was increased. This observation supports the assumption that β‐adrenoceptors can be desensitized or inactivated during continued exposure to agonists. 5 It was shown for the first time that stimulation of β‐adrenoceptors enhances transmitter output from the motor nerve. It is proposed that these β‐adrenoceptors are of the β 1 ‐subtype and are localized on the endings of motor nerves. Circulating catecholamines may facilitate neuromuscular transmission by stimulation of presynaptic β‐adrenoceptors.