Premium
STIMULATION OF β 1 ‐ADRENOCEPTORS ENHANCES ELECTRICALLY EVOKED [ 3 H]‐ACETYLCHOLINE RELEASE FROM RAT PHRENIC NERVE
Author(s) -
Wessler I.,
Holzer G.,
Künster A.
Publication year - 1990
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1990.tb01261.x
Subject(s) - acetylcholine , phrenic nerve , stimulation , nerve stimulation , chemistry , electric stimulation , anesthesia , neuroscience , pharmacology , medicine , biology , respiratory system
SUMMARY 1. The effects of isoprenaline, noradrenaline and fenoterol on the electrically evoked release of [ 3 H]‐acetylcholine from the rat phrenic nerve were investigated. 2. Isoprenaline (0.1 μmol/L) and noradrenaline (1 μmol/L) enhanced evoked [ 3 H]‐acetylcholine release by about 90%, an effect which was abolished by CGP 20712A (0.1 μmol/L), a specific antagonist at β 1 ‐adrenoceptors. Noradrenaline still enhanced [ 3 H]‐acetylcholine release in the presence of phentolamine (1 μmol/L). 3. The enhancing effect of both isoprenaline and noradrenaline decreased at prolonged exposure times (24–32 min). A pre‐exposure of the tissue to a low concentration (0.01 μmol/L) of isoprenaline prevented the enhancing effect of 0.1 μmol/L isoprenaline. 4. Fenoterol, a specific agonist at β 2 ‐adrenoceptors, did not modify evoked [ 3 H]‐acetylcholine release. 5. The present results indicate the existence of facilitatory β 1 ‐adrenoceptors on the motor nerve. These receptors appear to be desensitized either by a high concentration of, or by a long exposure to, agonists. Under the present conditions noradrenaline enhances the release of newly synthesized transmitter mainly by stimulation of β‐adrenoceptors.