title: Mechanism responsible for alterations in numbers of autonomic nerve receptors in experimental asthma.
abstract: This study was designed to elucidate the mechanism responsible for alterations in the numbers of autonomic nerve receptors in experimental asthma. In the in vivo experiment, guinea pigs sensitized by exposure to aerosol of 2% ovalbumin for 7-8 min for 10 successive days were used as the experimental asthma group. The control group was exposed to saline. Beta-, alpha-1-adrenergic and muscarinic acetylcholine receptors in lung membranes were studied by direct binding techniques using l-3H-dihydroalprenolol, 3H-bunazosin and l-3H-quinuclidinyl benzilate, respectively. The experimental asthma group showed a 33% decrease in the number of beta-adrenergic receptors, a 37% increase in the number of alpha-1-adrenergic receptors and no change in the number of muscarinic acetylcholine receptors compared with the control group. The endogenous phospholipase activity was determined by high-performance liquid chromatography using tridecanoyl phosphatidylcholine as a substrate. The phospholipase activity in lung membranes in the experimental asthma group was elevated by 50% compared with that in the control group. Lung membrane phospholipid composition was analyzed by thin-layer chromatography with a flame ionization detector. In the experimental asthma group, the amounts of phosphatidylcholine and phosphatidylethanolamine decreased significantly compared with those in the control group. In the in vitro experiment after pretreatment of lung membranes with phospholipase A2, a decreased number of beta-adrenergic receptors, an increased number of alpha-1-adrenergic receptors and no change in the number of muscarinic acetylcholine receptors were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, University of Nagoya, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
authors.forename: F
authors.initials: F
authors.lastname: Taki
authors.forename: S
authors.initials: S
authors.lastname: Sugiyama
authors.forename: K
authors.initials: K
authors.lastname: Takagi
authors.forename: T
authors.initials: T
authors.lastname: Satake
authors.forename: T
authors.initials: T
authors.lastname: Ozawa
mesh_terms: D000818:Animals; D001249:Asthma / Q000201:enzymology / Q000209:etiology / Q000378:metabolism*; D004195:Disease Models, Animal; D006168:Guinea Pigs; D008168:Lung / Q000032:analysis / Q000201:enzymology / Q000378:metabolism; D008297:Male; D010740:Phospholipases / Q000378:metabolism; D010741:Phospholipases A / Q000494:pharmacology; D054467:Phospholipases A2; D010743:Phospholipids / Q000378:metabolism; D011942:Receptors, Adrenergic, alpha / Q000032:analysis / Q000187:drug effects; D011943:Receptors, Adrenergic, beta / Q000032:analysis / Q000187:drug effects; D011976:Receptors, Muscarinic / Q000032:analysis / Q000187:drug effects; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism*
chemical_list: D010743:Phospholipids; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D011976:Receptors, Muscarinic; D017981:Receptors, Neurotransmitter; D010740:Phospholipases; D010741:Phospholipases A; D054467:Phospholipases A2