Cardiac norepinephrine releasing action of kynuramine, an endogenous diamine derived from L-tryptophan.

Kynuramine, an endogenous metabolite of L-tryptophan, was found to function as an indirectly acting sympathomimetic amine in rat atria in vitro. Kynuramine released tritium from atria preloaded with [3H]norepinephrine (NE), an effect which was blocked completely by pretreatment with reserpine or 6-hydroxydopamine. Release by kynuramine was calcium-independent and was potentiated by inhibition of monoamine oxidase but was only partially sensitive (50%) to inhibition by cocaine (10(-4)M). The ability of kynuramine to enter cardiac cells was demonstrated in whole atria by measuring its intracellular deamination rate by monoamine oxidase. Blockade of neuronal uptake (cocaine) and extraneuronal uptake (SKF 550) had no effect upon this measure. It is concluded that knyuramine releases cardiac NE, in part, by a cocaine-sensitive mechanism but that the process operating for the membrane transport of kynuramine in both neuronal and non-neuronal cells remains uncertain. The data are discussed in relation to the possible cardiac consequences of L-tryptophan ingestion in man.