Figure 9.

AAV-mediated silencing of pGC-A or CSE significantly attenuated E2-induced vasodilation. Mice at 8 weeks of age were injected from the tail vein with AAV-control-shRNA (5.0*10¹¹ v.g), AAV-pGC-A-shRNA (5.0*10¹¹ v.g), AAV-CSE-shRNA (7.5*10¹¹ v.g). A–D, after 4 weeks, the aortae were dissected out and pretreated for 30 min with 200 mm l-NNA (NO inhibitor) and 10 mm Indo (prostaglandin synthesis inhibitors) and preconstricted with Phe (10⁻⁶ m) before testing with Ach (10⁻⁵ m) (mean ± S.D.; n = 5 independent experiments; ***, p < 0.001 versus CON; one-way ANOVA followed by the post hoc LSD test). E–H, knockdown of pGC-A or CSE expression significantly attenuated E2-induced vasodilation (mean ± S.D.; n = 5 independent experiments; ***, p < 0.001 versus CON; one-way ANOVA followed by the post hoc LSD test).