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. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Hypertension. 2021 May 3;77(6):2117–2126. doi: 10.1161/HYPERTENSIONAHA.120.16911

Figure 5. Combined ERα and MR Deletion in EC Negates Improved EC-MR-KO Endothelial Dependent Vasodilation by decreasing NO Contribution.

Figure 5.

(A) Representative images of PCR confirming gene recombination using DNA from EC-rich lung tissue from EC-MR-WT/KO and EC-ERα/MR-WT/KO mice. PCR indicates the wild type MR allele, floxed MR allele and recombined MR (top image) and wild type ERα, floxed ERα, and recombined ERα (bottom image). (B) ACh vasodilation is impaired in EC-ERα/MR-KO females. EC-MR-WT and KO curves from Figure 1A are replotted here in black and compared directly. 2-Way repeated measures ANOVA, Bonferroni post hoc. *p<0.05 EC-MR-WT vs EC-MR-KO; #p<0.05 EC-ERα/MR-WT vs EC-ERα/MR-KO; $p<0.05 EC-ERα/MR-KO vs EC-MR-KO. (C) Nitric oxide synthase (NOS) contribution to vasodilation in obese WT females. (D) NOS contribution in obese EC-MR-KO females and EC-ERα/MR-KO females. (E) NOS contribution to vasodilation was calculated as difference in the area under the curve (dAUC) between ACh dilation and ACh+NOS inhibition in each geneotype. WT females were combined from both WT groups (EC-MR-WT and EC-ERα/MR-WT). *p<0.05, one-way ANOVA with Sidak post-hoc.