"FALSE NEUROCHEMICAL TRANSMITTERS" AND THE MECHANISM OF SYMPATHETIC BLOCKADE BY MONOAMINE OXIDASE INHIBITORS

The hypothesis is proposed that the partial sympathetic blockade observed after chronic inhibition of monoamine oxidase or after administration of large doses of tyramine may be the consequence of replacement of norepinephrine by a false, inactive neurochemical transmitter.

Abstract

Following administration of tyramine-H 3 or m -tyramine-H 3 the β-hydroxylated derivatives of these amines, octopamine-H 3 and m -octopamine -H 3 , are rapidly formed in the heart and salivary gland. Formation of the β - hydroxylated derivatives is enhanced by inhibition of monoamine oxidase, but α-methyloctopamine-H 3 formation from α-methyltyramine-H 3 is uninfluenced. Octopamine-H 3 formation and endogenous octopamine accumulation after monoamine oxidase inhibition are largely prevented by chronic sympathetic denervation. Octopamine in tissues is released by sympathetic nerve stimulation, but this amine is relatively inactive. The hypothesis is proposed that the partial sympathetic blockade observed after chronic inhibition of monoamine oxidase or after administration of large doses of tyramine may be the consequence of replacement of norepinephrine by a false, inactive neurochemical transmitter.