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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Circulation. 2014 Mar 17;129(13):1428–1439. doi: 10.1161/CIRCULATIONAHA.113.004146

Figure 3.

Figure 3

Endothelial deletion of LKB1 impairs eNOS-dependent vasodilation. A, PE-induced contraction force in aortic rings from LKB1endo−/− and WT mice. Vascular reactivity of LKB1endo−/− and WT aortic rings to ACh without (B) or with L-NAME pretreatment (100 μM) for 30 min (C). D, Vascular reactivity of LKB1endo−/− and WT aortic rings to SNP. Vascular reactivity of LKB1endo−/− and WT mesenteric vessels to ACh without (E) or with L-NAME pretreatment (F). Aortic rings from LKB1endo−/− and WT mice were contracted with PE (10− M) and then incubated with L-NAME (100 μM) to remove basal NO synthesis. A representative contraction curve is shown (G) and the force (H) was quantified. Data are mean ± SEM, n = 5 animals and two aortic rings per animal. *p < 0.05 vs. WT.