Figure 4.

Vascular Arginase and Superoxide Mediate Endothelial Dysfunction Induced by C19-RBCs

Endothelium-dependent relaxation induced by acetylcholine (ACh) in rat aorta following incubation of C19-RBCs in the absence or presence of (A) the arginase inhibitor 2(S)-amino-6-boronohexanoic acid (ABH) (n = 8), (B) the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPOL) (n = 7), or (C) the NOX inhibitor apocynin (n = 7). Endothelium-independent relaxation was evaluated by 1 dose of sodium nitroprusside (SNP) at the end of the experiment in the absence or presence of (D) ABH (n = 8), (E) TEMPOL (n = 7), or (F) apocynin (n = 7). ( ) indicates that compounds were applied after the 18-hour incubation to selectively target the vasculature. ∗P < 0.05 vs C19-RBCs with 2-way analysis of variance matched for both concentration and relaxation (A, B, C), paired Student's t-test (D), or Wilcoxon test (E, F). Values are expressed as mean and SD (A-D) or median (Q1-Q3) (E, F).