Nath P, Joshi A P, Agrawal K P
J Allergy Clin Immunol. 1983 Oct;72(4):351-8. doi: 10.1016/0091-6749(83)90499-2.
To elucidate the biochemical basis of airway hyperreactivity, we studied the relationships between in vivo airway sensitivity of guinea pigs to histamine and their tracheal beta-adrenergic binding sites, Ca++- and (Na+-K+)-ATPase activities, and composition of phospholipids. The relationships between tracheal and plasma phospholipids were also examined. beta-Adrenergic receptor binding with 3H-dihydroalprenolol in tracheal tissue showed an inverse relationship with in vivo airway sensitivity to histamine. Among the phospholipids, tracheal phosphatidyl ethanolamine content varied inversely with in vivo airway sensitivity, whereas tracheal and plasma lysophosphatidyl choline contents showed a direct correlation with airway sensitivity. A significant direct correlation was also observed between tracheal and plasma lysophosphatidyl choline levels. Both Ca++-ATPase and (Na+-K+)-ATPase activities increased with increasing airway sensitivity. These enzymes showed inverse correlations with phosphatidyl ethanolamine content and direct correlations with lysophosphatidyl choline content. Our data suggest that increased lysophosphatidyl choline may cause various biochemical changes associated with airway hyperreactivity.
