Figure 2.

Endothelium‐dependent dilation in young and old untreated and old rapamycin‐treated mice. (A) Dose responses to acetylcholine in the absence or presence of the nitric oxide synthase inhibitor, L‐NAME, in carotid arteries from young (YC) (N = 6) and old (OC) (N = 9) untreated mice. (B) Dose responses to acetylcholine in the absence or presence of L‐NAME in carotid arteries from OC (N = 9) and old rapamycin (ORAP) (N = 9)‐treated mice. (C) Dose responses to acetylcholine in the absence or presence L‐NAME in carotid arteries from YC (N = 9) and young rapamycin (YRAP) (N = 9)‐treated mice. (D) Dose responses to the endothelium‐independent vasodilator, sodium nitroprusside, in carotid arteries from YC, OC, YRAP, and ORAP mice (N = 4–8/group). * denotes group difference from YC, † denotes group differences from OC, and § denotes difference with L‐NAME from ACh alone. Differences in dose responses were assessed by repeated‐measures ANOVA. (E) Total (open bars) and the ratio of ser1177 phosphorylated (P‐) to total (hashed bars) expression of endothelial nitric oxide synthase (eNOS) in aortas excised from young and old untreated and rapamycin‐treated mice (N = 4–6/group), P = 0.1 denotes tendency for difference in the ratio for young vs. old and old vs. old Rap. Blot images are provided next to summary data. Differences were assessed by one‐way ANOVA. Data are means ± SEM, P ≤ 0.05