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Significance Vasodilation is impaired in the postischemic heart due to loss of endothelial nitric oxide synthase (eNOS) function; however, the central trigger of this endothelial dysfunction is unknown. We observe that near total depletion of the eNOS substrate NADPH occurs in postischemic endothelium, triggering eNOS dysfunction and limiting rescue of its essential cofactor BH4 . This NADPH depletion was shown to be due to marked activation of the NAD(P)ase activity of CD38 and could be prevented by its inhibition or genetic knockdown. Thus, CD38 activation with pronounced NADPH depletion is first identified as a critical trigger of postischemic endothelial dysfunction, and this presents a novel therapeutic target for the treatment of unstable coronary syndromes and prevention of coronary disease.

Depletion of NADP(H) due to CD38 activation triggers endothelial dysfunction in the postischemic heart