Fig. 3.

Endothelial expression of Cav-1 impairs eNOS-dependent vasodilation. (A) Representative bioassay trace from WT littermate (intermittent line) and Cav-1 TG (solid line) mice. Aortic rings were precontracted with PE, and ACh-induced dilations were examined. (B) Statistical analysis of the full dose–response curves to ACh demonstrates a 10-fold change in the EC₅₀ value for ACch in Cav-1 TG mice. (C) Basal eNOS activation is reduced in Cav-1 TG. Vessels were contracted with PE and then incubated with a NOS inhibitor L-NAME to remove basal NO synthesis. (D) Cav-1 TG mice show a deficiency in basal NO synthesis. (E and F) The deficit in eNOS activation does not influence the ability of the vessels to contract to PE or to relax to the NO donor drug, SNP. Data are mean ± SEM, with n = 5 animals and two aortic rings per animal. *, P < 0.05.