PMID- 7513131
OWN - NLM
STAT- MEDLINE
DCOM- 19940520
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 266
IP  - 3 Pt 1
DP  - 1994 Mar
TI  - Increased acetylcholine release in tracheas from allergen-exposed IgE-immune 
      mice.
PG  - L263-70
AB  - 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)
FAU - Larsen, G L
AU  - Larsen GL
AD  - Department of Pediatrics, National Jewish Center for Immunology and Respiratory 
      Medicine, Denver, Colorado.
FAU - Fame, T M
AU  - Fame TM
FAU - Renz, H
AU  - Renz H
FAU - Loader, J E
AU  - Loader JE
FAU - Graves, J
AU  - Graves J
FAU - Hill, M
AU  - Hill M
FAU - Gelfand, E W
AU  - Gelfand EW
LA  - eng
GR  - AI-26490/AI/NIAID NIH HHS/United States
GR  - AI-29704/AI/NIAID NIH HHS/United States
GR  - P01-HL-36377/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Allergens)
RN  - 0 (Autoreceptors)
RN  - 0 (Epitopes)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Receptors, Muscarinic)
RN  - 0W5ETF9M2K (Methacholine Chloride)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/*metabolism/pharmacology
MH  - Allergens/*immunology
MH  - Animals
MH  - Autoreceptors/metabolism
MH  - Electric Stimulation
MH  - Epitopes
MH  - Female
MH  - Immunoglobulin E/*immunology
MH  - Immunoglobulin G/immunology
MH  - Methacholine Chloride/pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Muscle, Smooth/immunology/metabolism
MH  - Receptors, Muscarinic/metabolism
MH  - Trachea/*immunology/*metabolism
EDAT- 1994/03/01 00:00
MHDA- 1994/03/01 00:01
CRDT- 1994/03/01 00:00
PHST- 1994/03/01 00:00 [pubmed]
PHST- 1994/03/01 00:01 [medline]
PHST- 1994/03/01 00:00 [entrez]
AID - 10.1152/ajplung.1994.266.3.L263 [doi]
PST - ppublish
SO  - Am J Physiol. 1994 Mar;266(3 Pt 1):L263-70. doi: 10.1152/ajplung.1994.266.3.L263.