Fig. 10
Defective autophagy in VSMCs increases the level of basal NO, stimulated NO release, and phosphorylated eNOS in the aorta without affecting exogenous NO-mediated relaxation. Force development after addition of 2 µM PE in aortic segments of Atg7F/F SM22α-Cre+ (F/F) and Atg7+/+ SM22α-Cre+ (+/+) mice in the absence (a) or presence (b) of 300 µM L-NAME to calculate amounts of basal NO release (c). Relative concentration–response curves of relaxations elicited by acetylcholine (ACh) of Atg7F/F SM22α-Cre+ (F/F) and Atg7+/+ SM22α-Cre+ (+/+) aortic segments (d), fitted IC50 (e) and maximal relaxation values (f). Relative concentration–response curves of relaxations elicited by DEANO of Atg7F/F SM22α-Cre+ (F/F) and Atg7+/+ SM22α-Cre+ (+/+) aortic segments (g), fitted IC50 (h) and maximal relaxation values (i) (n = 7). Western blot (j) analysis of eNOS and (p)-eNOS with quantification relatively expressed to β-actin (k, i) (n = 6). Independent students t test. *p < 0. 05, **p < 0.01