Interaction of nicotine and other amines with the endocytic and exocytic functions of macrophages.
Nicotine inhibits endocytosis and stimulates exocytosis in macrophages. At the same concentrations (5-15 mM) that the alkaloid exerts these effects, it is also vacuologenic. Consideration was given to one hypothesis that the membrane internalization was a result of surfactant activity. Nicotine was found to have surfactant properties. Studies involving measurements of the contact angles of a sessile drop of saline on cell monolayers suggested that nicotine increased the hydrophilicity of the membrane. The possibility has been considered that this may be indicative of membrane expansion and that this expansion leads to collapse and vesicle formation. This would be analogous to the effects of surface-active amines (e.g., local anesthetics, tranquilizers, antihistamines) on lipid monolayers and erythrocytic membranes. It is suggested that if such a mechanism does occur, then the possibility exists for a variety of amines to nonspecifically alter membrane and receptor availability of the macrophage.
D000818:Animals; D002462:Cell Membrane / Q000187:drug effects; D004705:Endocytosis / Q000187:drug effects; D005089:Exocytosis / Q000187:drug effects; D005260:Female; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D051379:Mice; D009538:Nicotine / Q000494:pharmacology*; D011247:Pregnancy; D013501:Surface-Active Agents / Q000494:pharmacology; D014617:Vacuoles / Q000187:drug effects
D013501:Surface-Active Agents; D009538:Nicotine