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. Author manuscript; available in PMC: 2016 Jan 31.
Published in final edited form as: Hypertension. 2014 Dec 1;65(2):385–392. doi: 10.1161/HYPERTENSIONAHA.114.04285

Figure 5.

Figure 5

Dose-dependent reversal of PE-induced vasoconstriction in mice with WT vs. redox-dead (C42S) PKG1α (n=4-16/group). The absence of PKG1α redox sensitivity did not alter CXL-1020 vasodilation dose-sensitivity in both A) conduit (aorta) and B) resistance (B) (mesenteric) arteries. In both cases, application of ODQ suppressed CXL-1020 vasodilation. C) Non-reducing gel electrophoresis for PKG1α monomer and dimer in response to H2O2 (positive control) versus CXL-1020 (the latter tested in both wild type (WT) and PKG1αC42S mutant mesenteric arteries. CXL-1020 did not stimulate dimer formation.