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Effect of cholinergic and cholinergic blocking drugs on decamethonium uptake by slices of mouse kidney.

The accumulation of decamethonium by mouse kidney slices was investigated with particular reference to the possibility that this agent uses a choline transport system. Slices of mice kidneys were incubated (1 hour) in Krebs-Ringer bicarbonate medium (37°, pH 7.4) containing 14C-decamethonium (2 × 10-6M) with or without the addition of other drugs. Choline and neostigmine stimulated decamethonium uptake at relatively low concentrations (10-3M and 3 × 10-3M choline, 5 × 10-5M and 10-4M neostigmine), whereas both agents at higher concentrations (3 × 10-2M choline, 10-3M and 10-2M neostigmine) depressed the uptake. Hemicholinium-3 (10-3M), atropine (2 × 10-5M) and physostigmine (2 × 10-4M) inhibited decamethonium uptake, indicating that these agents in addition to choline and neostigmine share a common transport mechanism with decamethonium. The initial decamethonium influx (3 minutes incubation) could be stimulated by pre-incubating the slices (1 hour) with 10-3M choline or 3 × 10-4M neostigmine (in the absence of decamethonium) before transfer to a final medium containing only decamethonium. Stimulation can thus be interpreted as an example of accelerative exchange diffusion, which should mean that efflux of choline or neostigmine accumulated by the slices accelerates decamethonium influx. It is concluded that decamethonium uses a specialized transport system, which seems to involve a choline carrier and to be in part at least identical with the system responsible for organic cation secretion by the intact kidney.