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. 2012 Nov 15;61(12):3219–3227. doi: 10.2337/db12-0162

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© 2012 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by -nc-nd/3.0/ for details.

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FIG. 3. — Vasoconstriction and vasorelaxation responses of mesenteric arteries (MA) and DHE fluorescence of MA after treatment with TEMPOL. Control, DIO Psgl-1^+/+, and Psgl-1^−/− mice (n = 5–7 per group). A: Concentration response to NE. B: Concentration response to SNP. C: Concentration response to Ach. D: Concentration response to Ach after preincubation in l-NAME. E: l-NAME–sensitive maximal vasorelaxation responses to Ach. F: Concentration response to Ach of MA from DIO Psgl-1^+/+ after treatment with TEMPOL. G: Concentration response to SNP of MA from DIO Psgl-1^+/+ after treatment with TEMPOL. H: DHE fluorescence of MA from DIO Psgl-1^+/+ without (left) and with (right) TEMPOL treatment. Scale bar: 50 μm. *P < 0.05 compared with DIO Psgl-1^−/− mice, control Psgl-1^−/− mice, and control Psgl-1^+/+ mice. #P < 0.05 compared with vessels without TEMPOL treatment. (A high-quality color representation of this figure is available in the online issue.)

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