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Exercise catecholamine concentrations inhibit acetylcholine release in airways
Author(s) -
ROBINSON N. E.,
ZHANG XY.,
LEBLANC P. H.,
DERKSEN F. J.
Publication year - 1995
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/j.2042-3306.1995.tb04886.x
Subject(s) - trachealis muscle , acetylcholine , chemistry , guanethidine , prazosin , endocrinology , medicine , muscarinic antagonist , atropine , antagonist , catecholamine , contraction (grammar) , muscle contraction , stimulation , membrane potential , biochemistry , receptor , charybdotoxin
Summary We determined the effects of exercise induced concentrations of epinephrine (E) and norepinephrine (NE) on acetylcholine (ACh) release and smooth muscle contraction. To determine ACh release, trachealis strip bundles were suspended in 2 ml tissue baths in the presence of neostigmine (10 −6 M), guanethidine (10 −5 M) and atropine (10 −7 M), and stimulated by electrical field stimulation (EFS; 20 V , 0.5 ms, 0.5 Hz, for 15 min). EFS‐induced ACh release was measured by high‐performance liquid chromatography coupled with electrochemical detection. Concentration responses to E and NE (10 −8 to 10 −5 M) were determined. In time‐control tissues, ACh release averaged 8.2 ± 0.9 pmol/g/min. Epinephrine caused significant inhibition of ACh release at concentrations of 10 −7 M or greater and NE at 10 −6 M or greater. E‐ and NE‐induced inhibition of ACh release was attenuated by the α 2 ‐adrenoceptor antagonist idazoxan (10 −6 M) but not by the α 2 ‐antagonist prazosin (10 −6 M) nor the β‐antagonist propranolol (10 −6 M). We determined if E and NE had inhibitory actions on smooth muscle by examining their effect on the ACh concentration‐response curve of trachealis. E (10 −6 M) inhibited contraction only at 10 −7 M ACh, i.e. when muscle tension was low. NE had no effect. Exercise induced concentrations of E inhibit cholinergically mediated bronchospasm primarily by α 2 ‐mediated prejunctional inhibition of ACh release and, to a lesser degree, by a post junctional effect on airway smooth muscle. NE only inhibits ACh release but not significantly at the concentrations achieved during exercise.