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Role of the alveolar macrophage in the induction of pulmonary phospholipidosis by chlorphentermine. II. Drug uptake into cells in vitro.

This study was conducted to further assess the role of the alveolar macrophage in the induction of pulmonary phospholipidosis by the cationic amphiphilic drug, chlorphentermine (CP). Alveolar macrophages were collected from normal rats by pulmonary lavage, allowed to attach to glass cover slips and incubated with CP in vitro at 37 degrees C. The uptake of CP was measured using [14C]CP. Uptake is rapid, reaching equilibrium by 2 min resulting in the concentration of CP within the cells. The process is temperature-dependent being depressed markedly at 2 degrees C. Two components of uptake were identified. Below 0.2 mM CP, a carrier-mediated mechanism and diffusion are involved whereas, at concentrations above 0.2 mM, the carrier is saturated and diffusion predominates, with the intracellular binding of CP to membranes probably responsible for the striking sequestration. The carrier-mediated component obeys Michaelis-Menten kinetics, does not appear to require Na+ and is not affected by metabolic inhibitors. This is consistent with the concept that the process occurs by facilitated diffusion. Metabolism of CP does not play a role in the accumulation of the drug. The transport system is different from those involved in glucose, nucleoside or amino acid uptake. Total initial uptake was inhibited by the three cationic amphilic drugs tested, iprindole, chlorcyclizine and imipramine indicating that cationic amphiphilic drugs may share a common uptake system.