Effect of Tetraethylammonium and N1-Methylnicotinamide on the Uptake of Decamethonium and Carbamoylcholine by Slices of Mouse Kidney
| Autor: | Jan Holm |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Niacinamide
medicine.medical_specialty Decamethonium Compounds Bicarbonate Stimulation Kidney Toxicology Mice chemistry.chemical_compound Decamethonium Internal medicine medicine Animals Incubation Pharmacology Carbon Isotopes Tetraethylammonium Tetraethylammonium Compounds Stimulation Chemical Endocrinology medicine.anatomical_structure chemistry Mouse Kidney Biophysics Carbachol N1 methylnicotinamide medicine.drug |
| Zdroj: | Acta Pharmacologica et Toxicologica. 30:89-96 |
| ISSN: | 0001-6683 |
| DOI: | 10.1111/j.1600-0773.1971.tb00637.x |
| Popis: | An investigation was performed to determine whether decamethonium and carbamoylcholine share a common transport mechanism with tetraethyl-ammonium and N1-methylnicotinamide in mouse kidney slices. Slices were incubated (1 hour) in Krebs-Ringer bicarbonate medium (37°, pH 7.4) containing 2 × 10-6M 14C-labelled decamethonium or carbamoylcholine both in the absence and presence of the drugs. Tetraethylammonium and N1-methylnicotinamide stimulated decamethonium uptake at relatively low concentrations (5 × 10-5M and 10-4M tetraethylammonium, 10-4M and 5 × 10-4M N1-methylnicotinamide), whereas both agents at higher concentrations (10-3M and 10-2M tetraethylammonium, 2 × 10-2M N1-methylnicotinamide) depressed the uptake. Tetraethylammonium (10-4M, 10-3M) and N1-methylnicotinamide (10-3M) also inhibited the uptake of carbamoylcholine. The initial decamethonium influx (3 minutes incubation) could be stimulated by pre-incubating slices (1 hour) with 3 × 10-4M tetraethylammonium or 5 × 10-4M N1-methylnicotinamide (in the absence of decamethonium) before being transferred to a final medium containing only decamethonium. Stimulation can thus be interpreted as an example of accelerative exchange diffusion, which should indicate that efflux of tetraethylammonium or N1-methylnicotinamide accumulated by the slices accelerates the influx of decamethonium. It is concluded that decamethonium and carbamoylcholine use a carrier mechanism which is also involved in tetraethylammonium and N1-methylnicotinamide transport. This transport mechanism is most likely in part at least, identical with that responsible for the secretion of tetraethylammonium and N1-methylnicotinamide (and other organic cations) by the intact kidney. |
| Databáze: | OpenAIRE |
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