The classic monoamine oxidase inhibitors (MAOIs) tranylcypromine (TCP) and phenelzine (PLZ) are powerful antidepressants that come with an equally powerful stigma, and are thus rarely prescribed—despite their well-established effectiveness. Some of these preconceptions appear to stem from unclarity, as the etiology of a rare but important side effect, ‘spontaneous hypertension’ (SH)—a significant increase in blood pressure absent dietary tyramine ingestion—remains improperly elucidated. This paper aims at uprooting some of the stigma surrounding MAOIs by advancing the trace amine (TA) theory as the causative underpinning of SH. This theory posits that SH results from the considerable influx of TAs observed following TCP- or PLZ-administration. TAs are known, albeit at greatly supraphysiological levels, to raise blood pressure on account of their propensity to exert potent indirect sympathomimetic effects; additionally, some research posits that TAs may induce vasoconstrictive effects partly or wholly separate therefrom, which would then constitute a second hypertensive mechanism. TAs are endogenous to the human body in low quantities. Both TCP and PLZ cause marked elevations of 2-phenylethylamine (PEA), meta- and para-tyramine (m-/p-TYR), octopamine (OA), and tryptamine (TRYP), following both acute and (sub)chronic administration. This paper holds that TYR plays a pivotal role in causing SH, due to its strong pressor effect. Cautious treatment of SH is advised, given its typically self-limiting nature. The risk of hypotensive overshoots must be taken into account. For severe cases, this paper urges reconsideration, following suitable confirmation trials, of antipsychotics (notably risperidone) as these agents may reduce striatal p-TYR levels.

经典的单胺氧化酶抑制剂 (MAOIs) 反苯环丙胺 (TCP) 和苯乙肼 (PLZ) 是强大的抗抑郁药，具有同样强大的耻辱感，因此很少开处方——尽管它们的有效性已得到证实。其中一些先入之见似乎源于不明确，因为罕见但重要的副作用“自发性高血压”（SH）的病因学——在没有饮食中摄入酪胺的情况下血压显着升高——仍未得到正确阐明。本文旨在通过将微量胺 (TA) 理论作为 SH 的病因基础，根除围绕 MAOI 的一些污名。该理论假定 SH 是由于在 TCP 或 PLZ 给药后观察到的 TA 大量涌入所致。TA 是已知的，尽管处于极大的超生理水平，由于他们倾向于发挥有效的间接拟交感神经作用而升高血压；此外，一些研究认为 TA 可能会引起部分或完全独立的血管收缩作用，这将构成第二种高血压机制。TA 是人体内源性的，数量很少。在急性和（亚）慢性给药后，TCP 和 PLZ 都会导致 2-苯乙胺 (PEA)、间和对酪胺 (m-/p-TYR)、章鱼胺 (OA) 和色胺 (TRYP) 显着升高. 本文认为TYR由于其强大的升压作用而在引起SH中起关键作用。鉴于其典型的自限性，建议谨慎对待 SH。必须考虑低血压超调的风险。对于严重的情况，本文敦促重新考虑，