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1 Department of Physiology, State University of New York, Upstate Medical Center, Syracuse, N. Y., and Department of Pharmacology, Tulane University Medical School, New Orleans, La.
An immediate inhibition of the renal tubular excretion of N-methylnicotinamide (NMN) and tetraethylammonium (TEA) occurred in dogs following intravenous injection of small single doses of a basic cyanine dye (# 863). A delayed and less striking inhibition of the tubular transport of TEA by the cyanine occurred in chickens when both substances were infused simultaneously into the renal portal circulation. The amount of cyanine excreted in the urine was extremely small, and unequivocal evidence of the renal tubular excretion of cyanine was not obtained.
Accumulation of high concentrations of cyanine in the renal tubular cells of the dog was demonstrated. Disappearance of the inhibitor from this site occurred at the same rate as did reversal of cyanine-induced inhibition of NMN transport in a previous study. Cellular fractionation studies showed most of the cyanine to be localized in mitochondria.
Several other cyanines and a styrylquinoline dye also were found capable of depressing the renal tubular transport of NMN.
Submitted on May 25, 1956