CHOLINESTERASE ACTIVITY IS SIMILAR IN C3H/HeJ AND A/J MICE AND DOES NOT ACCOUNT FOR THEIR DIFFERENT BRONCHOCONSTRICTOR RESPONSIVENESS

• Published in: Experimental lung research 1999, Vol.25 (5), p.367-378
• Main Author: Yonca Bulut, Steven R. Kleeberger, Carol A. Hirshman
• Format: Article
• Language: English
• Subjects: Acetylcholine - pharmacology; Acetylcholine; Acetylcholinesterase; Butyrylcholinesterase; Cholinergic Reactivity; Mouse; Acetylcholinesterase - blood; Air breathing; Airway Resistance - drug effects; Animals; Biological and medical sciences; Bronchial Hyperreactivity - chemically induced; Bronchial Hyperreactivity - enzymology; Bronchial Provocation Tests; Bronchoconstriction - drug effects; Butyrylcholinesterase - blood; Cholinesterase Inhibitors - pharmacology; Drug Interactions; Fundamental and applied biological sciences. Psychology; Male; Mice; Mice, Inbred C3H; Neostigmine - pharmacology; Respiratory system: anatomy, metabolism, gas exchange, ventilatory mechanics, respiratory hemodynamics; Species Specificity; Succinylcholine - pharmacology; Vertebrates: respiratory system
• ISSN: 0190-2148; 1521-0499
• DOI: 10.1080/019021499270132

Significant interstrain variation in airway responsiveness to acetylcholine (ACh) exists in inbred mouse strains. We hypothesized that part of the variation may be due to between - strain differences in cholinesterase activity. We asked if administration of neostigmine (an acetylcholinesterase inhibitor) and / or succinylcholine (an agent which competes for and inhibits butyrylcholinesterase) altered ACh responsiveness in hyporesponsive C3H/HeJ and hyperresponsive A/J mouse strains. Airway responses to ACh were measured by the airway pressure time index in the presence and absence of succinylcholine (10 mg/kg) and / or neostigmine (0.7 mg/kg). In addition, acetylcholinesterase and butyrylcholinesterase activity were directly measured. Acetylcholinesterase and butyrylcholinesterase inhibition increased airway responses to acetylcholine in both strains, but did not eliminate or decrease the differences in airway responsiveness to ACh previously seen in the two strains. Cholinesterase activities in the two strains were not significantly different. We conclude that differences in either acetylcholinesterase or butyrylcholinesterase in the A/J or C3H/HeJ mouse strains are unlikely to contribute to the differences in airway responsiveness to exogeneously administered cholinergic agonists.