Fig. 1: EC-specific deletion of Mtor, Rptor, or Rictor caused impaired relaxation of the artery accompanying decreased NO bioavailability.

a–c Endothelium-dependent vasodilation (EDD) and endothelium-independent vasodilation (EID) of the abdominal aortas of Mtor^EC−/−, Rptor (Rpt)^EC−/−, Rictor (Ric)^EC−/− mice and their wild type (WT) littermates were measured by transcutaneous ultrasound imaging (n = 5–6) and calculated as follows: EDD% = (D₁–D₀)/D₀ × 100; EID% = (D₂–D₀)/D₀ × 100. Where D₀ is the mean diameter of the murine abdominal aorta over three cardiac cycles at baseline, D₁ is the maximum systolic diameter after flow-mediated dilation, and D₂ is the maximum systolic diameter after nitroglycerin infusion. Shown to the right are representative images of the abdominal aortas. Scale = 0.5 mm. d–f The dose responses of aortic rings to 10⁻⁹–10⁻⁵ mol/L acetylcholine (Ach) were evaluated by Myograph (n = 5–8). g–i NO levels in the mouse serum was measured with a colorimetric reaction (n = 7–9). Error bars correspond to standard error of the mean (SEM). *p < 0.05; **p < 0.01; ***p < 0.001 vs. WT littermates; two-tailed unpaired t test.