Extended Data Fig. 7: Role of PKG1α in arterial relaxation by IDO1–cis-WOOH.

a, b Concentration–response curves to cis-WOOH after pretreatment of denuded mouse abdominal aortas with vehicle (filled squares) or the competitive cGMP PKG inhibitor RP-8-CPT-cGMP (a, open squares), or the competitive ATP binding PKG inhibitor KT 5283 (b, open squares). c, Relaxation of pre-constricted mouse mesenteric resistance arteries from LPS-treated wild-type (black) and PKG1α(C42S) knock-in mice (grey) by the nitric oxide donor DEANO (n = 4 for both genotypes). d, e, IDO activity in kidney homogenate (d) and plasma kynurenine-to-tryptophan ratio (as an index of systemic IDO activity) (e) obtained from wild-type (WT) or PKG1α(C42S) knock-in (KI) mice after treatment with LPS. f, Dimerization of PKG1α in human smooth muscle cells induced by Trp, 1 μM H₂O₂ or both, in the presence (+) or absence (–) of the IDO1 inhibitor epacadostat (n = 5). Cells were pretreated with (+) or without (–) 100 ng ml⁻¹ rhIFN-γ for 72 h. Data show mean ± s.e.m. of 5 (a, f), 4 (b, c, e) or 3–4 (d) independent experiments. *P ≤ 0.05 using repeated measures two-way ANOVA with Šidák multiple comparison post hoc test (a–c), Kruskal–Wallis with Dunn’s test (f). NS, not significant (Mann–Whitney).