We found that aortic arches from TRPC1 knockout mice (on a 129S background) exhibited the same TBI-mediated endothelial dysfunction as the 129S control mice (10 μM acetylcholine-induced dilation of 56.1 ± 4.1% in sham 129S-TRPC1 KO versus 27.9 ± 7.4% in TBI-129S-TRPC1 knockout mice compared to 58.0 ± 4.0% in sham versus 32.3 ± 6.8% in TBI in 129S control mice; Fig. 4c and Fig. 3c). This evidence concerns the gene TRPC1 and endothelial dysfunction.