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- Charles J Lowenstein and Thomas Michel.
- Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
- J. Clin. Invest. 2006 Aug 1;116(8):2075-8.
AbstractIn 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?
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