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. 2015 Jan 7;35(3):512–520. doi: 10.1038/jcbfm.2014.226

Figure 1.

Figure 1

Simvastatin (SV) improved cerebrovascular reactivity in transforming growth factor-β1 (TGF) mice. The impaired dilatory responses of isolated arteries to acetylcholine (ACh) (A) and calcitonin gene-related peptide (CGRP) (B) in TGF mice (▴, n=5) relative to wild-type controls (WT, ●, n=3) were normalized in SV-treated TGF (△, n=5) mice. Similarly, the basal nitric oxide (NO) synthesis, measured through NO synthase (NOS) inhibition with Nω-nitro-L-arginine (L-NNA) (C, 10−5 mol/L) was fully restored by SV treatment (△). TGF mice did not display perivascular amyloid deposits as seen with Thioflavin-S staining, the brighter segments correspond to small pieces of the attached pial membrane (D). MCA, middle cerebral artery; PCA, posterior cerebral artery. *P<0.05, **P<0.01, ***P<0.001 compared with WT; †P<0.05, ††P<0.01, †††P<0.001 compared with SV-treated TGF mice; ★P<0.05 compared with WT and SV-treated TGF mice.