Abstract
In this issue of the JCI, a study by Cauwels and colleagues suggests a central role for eNOS, the endothelial isoform of nitric oxide synthase, as a mediator of anaphylaxis (see the related article beginning on page 2244). Why is an enzyme originally described as a physiological mediator of vascular homeostasis implicated in the spectacular vascular collapse that is characteristic of anaphylaxis? And is the eNOS involved in anaphylaxis necessarily exerting its effect solely in the vascular endothelium, or might this “endothelial enzyme” actually be playing a more fundamental role in an entirely different tissue? After all, what’s in a name?
Authors
Charles J. Lowenstein, Thomas Michel
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