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. Author manuscript; available in PMC: 2014 Jul 15.
Published in final edited form as: Hypertension. 2011 Aug 1;58(3):431–438. doi: 10.1161/HYPERTENSIONAHA.111.172338

Figure 6.

Figure 6

Effect of Pin1 gene deletion on vascular endothelial NO synthase (eNOS) function and systolic blood pressure in mice. A, Representative Western blot showing aortic eNOS Ser116 phosphorylation. B, Aortic NO production as measured by Nω-nitro-l-arginine (LNNA)–sensitive 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM) fluorescence. C, Aortic relaxation responses to acetylcholine after contraction with phenylephrine in the absence and presence of NO synthase (NOS) inhibition (LNNA). Relaxation to 100% represents a full return to a passive tension of 0.75 g. D, Systolic blood pressure in Pin1 wild-type (WT) and knockout (KO) mice. Results are expressed as mean±SEM (n>5 mice for each group). *P<0.05 vs Pin1 WT.