Some Aspects of the Enzymic Inactivation of Sympathomimetic Amines

Abstract

This review seeks to discuss the possible importance of monoamine oxidase (MAO) and semicarbazide-sensitive amine oxidase (SSAO) in terminating the effects of released sympathetic transmitters and in the inactivation of endogenous or administered sympathomimetic amines with particular reference to some aspects of the cardiovascular system. Use of in vitro preparations of blood vessels and of other smooth muscles, such as vas deferens and anococcygeus, has thrown light on possible roles for these deaminating enzymes, even in the inactivation of noradrenaline, while the new reversible inhibitors of MAO-A show promise as antidepressants with a reduced risk of hypertensive crises following the ingestion of tyramine-containing food. However, the role of SSAO in the inactivation of amines remains an enigma, even though much is now known of its biochemical nature. While the pharmacological responses to amine substrates can be potentiated by inhibition of SSAO, there is a suspicion that it is product rather than substrate that is more important.

Semicarbazide‐sensitive amine oxidase: role in the vasculature and vasodilation after in situ inhibition

“…As is apparent, some of these are also MAO substrates, indicating that the affinity of both enzymes for aromatic amines tends to overlap. In contrast to MAO, it is unlikely that SSAO is involved in the inactivation of sympathomimetic amines (Callingham, 1987).…”