Increased acetylcholine release in tracheas from allergen-exposed IgE-immune mice.
Increased release of acetylcholine (ACh) from airway parasympathetic nerve endings is one mechanism that may contribute to increases in airway responsiveness in immunoglobulin E (IgE)-immune allergen-exposed animals. We measured ACh released from murine tracheas following electrical field stimulation in vitro. BALB/c mice were immunized by exposure to an aerosol of 1% ovalbumin in sterile phosphate-buffered saline for 20 min/day for 10 days. At this time, levels of ovalbumin-specific IgE were proportionately higher than ovalbumin-specific IgG. As a control, nonimmune mice were similarly exposed to phosphate-buffered saline alone. Forty-eight hours after the last aerosol, tracheas were removed for assessment of either the contractile responses to electrical field stimulation and a cholinergic agonist (methacholine or ACh) or release of ACh produced by electrical field stimulation. ACh in the bath was measured using high-performance liquid chromatography with electrochemical detection. The stimulation frequencies causing one-half the maximal contractile response to electrical field stimulation were 4.1 +/- 0.2 and 2.8 +/- 0.2 Hz (P = 0.0001) for nonimmune and immune mice, respectively, whereas the molar concentrations of methacholine causing one-half of the maximal contractile response did not significantly differ. In addition, the dose-response curves of immune and nonimmune tracheas to ACh were superimposable. A significant increase in ACh release was demonstrated at both 10 and 20 Hz in tracheas from immune mice. ACh release (pmol.g tissue-1.min-1) from nonimmune and immune murine tracheas, respectively, were 140 +/- 8 and 205 +/- 22 (P = 0.013) at 10 Hz and 147 +/- 13 and 227 +/- 14 (P = 0.008) at 20 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)
Larsen
G L
GL
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado.
Fame
T M
TM
Renz
H
H
Loader
J E
JE
Graves
J
J
Hill
M
M
Gelfand
E W
EW
D000109:Acetylcholine / Q000378:metabolism* / Q000494:pharmacology; D000485:Allergens / Q000276:immunology*; D000818:Animals; D017660:Autoreceptors / Q000378:metabolism; D004558:Electric Stimulation; D000939:Epitopes; D005260:Female; D007073:Immunoglobulin E / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D009130:Muscle, Smooth / Q000276:immunology / Q000378:metabolism; D011976:Receptors, Muscarinic / Q000378:metabolism; D014132:Trachea / Q000276:immunology* / Q000378:metabolism*
D000485:Allergens; D017660:Autoreceptors; D000939:Epitopes; D007074:Immunoglobulin G; D011976:Receptors, Muscarinic; D016210:Methacholine Chloride; D007073:Immunoglobulin E; D000109:Acetylcholine