Figure 4

CD73 deficiency does not aggravate angiotensin II induced vascular inflammation in mice. (A–E) Investigating the immune cell distribution numbers within the vessel wall, we could not detect any difference in total immune cells (A), myeloid (B) or lymphoid (C) cells between CD73 wildtype (grey) and CD73^−/− animals (red) after 10 days of angiotensin II treatment. The same was true for macrophages and neutrophils (D) or T and B cells (E) when comparing CD73 wildtype (grey) and CD73^−/− animals (red) after angiotensin II exposure. (F) Vessel area was determined by axial FLASH scans via MRI. Quantification revealed no differences between CD73 wildtype (grey) and CD73^−/− (red) mice. (G) Vessel strain, determined by ultrasound examination, showed no differences between CD73 wildtype (grey) and CD73^−/− (red) animals. (H) Blood flow velocity, also determined by ultrasound examination, again showed no differences between the CD73 wildtype (grey) and CD73^−/− (red) animals. (I) Temporal development of systolic blood pressure in CD73 wildtype (grey) and CD73^−/− (red) mice after minipump implantation with angiotensin II (at day 0). (J) Isolated immune cells from the aorta were incubated with ATP and the degradation products (e.g. AMP) were determined via UPLC measurements. All data sets are mean values ± SD of n = 39–47 (A), n = 39–47 (B), n = 39–47 (C), n = 42–54 (D), n = 42–54 (E), n = 36–42 (F), n = 44–48 (G), n = 44–48 (H) and n = 6 (I).