question: The vascular endothelium plays a crucial role to regulate vascular tone Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is known to cause vascular endothelial dysfunction However, the long-term effects of SARS-CoV-2 in resistance vessels remains unknown This study is designed to test whether endothelium-dependent vasodilation in human arterioles remains impaired after clearance of SARS-CoV-2 virus Fresh human adipose tissues were obtained as discarded surgical specimens from control subjects (n=15, no SARS-CoV-2 exposure, 46 7±4 years) and previously SARS-CoV-2 positive subjects (PSPSs: n=8, 35 8±3 8 years) Among PSPSs, the time between positive and negative SARS-CoV-2 test results was ≤3 months (n=6) or 8 months (n=2) Isolated arterioles (100-200 µm) were cannulated under 60 mmHg and examined for diameter changes to acetylcholine (ACh;10?9 to 10?5 M) and sodium nitroprusside (SNP: 10?9 to 10?4 M) using videomicroscopy Flow-mediated dilation (FMD) was recorded at steady-state during graded increases in intraluminal pressure gradients (5-100 cm H2O) Dilation to ACh and FMD in arterioles from PSPSs was significantly reduced (ACh max dilation at 10?5 M: 60±6% vs 92 8±3 9% in control, n=7-8, P&lt;0 001;FMD max dilation at 100 cm H2O: 39 9±5 7% vs 85 8±1 8% in control, n=6-8, P&lt;0 001, Fig 1) while endothelial-independent dilation in response to SNP was not different between groups (max dilation at 10-4 M: 86 6±2 7% vs 92 3±2 1% in control, n=5) To compare time-dependent effects of previous SARS-CoV-2 infection, we compared max dilator capacity vs time after exposure (Fig 2) At ≤3 months post exposure, FMD was significantly impaired (% max dilation: 26 7±7 4, n=5) whereas at 8 months endothelial function began to normalize (% max dilation: 41 8±17 6, n=2) In conclusion, we observed significantly reduced endothelial-dependent dilation months after exposed to SARS-CoV-2 Our data suggests SARS-CoV-2 may cause long-term endothelial dysfunction in human arterioles