Acute modulation of endothelial Akt/PKB activity alters nitric oxide–dependent vasomotor activity in vivo
J. Clin. Invest. Zhengyu Luo, et al. 106:493 doi:10.1172/JCI9419 [
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Figure 5dn-Akt attenuates aortic relaxations ex vivo in response to the endothelium-dependent agonist Ach, but not in response to SNP. Mouse aortae were cannulated and infused with adenoviral constructs that express either β-gal or dn-Akt, and vessels were placed into culture overnight. (
a) Specific and efficient adenovirus-mediated gene transfer to the endothelium as determined by β-gal expression detected by X-gal staining from a representative en face view. The arrow indicates the direction of flow. (
b) Cross section of vessel demonstrating that β-gal expression is detected in the endothelium, but not in medial smooth muscle cells or adventitia (A). L, lumen. Parts
a and
b are representative of three aortae. Bars represent 250 and 50 μm in
a and
b, respectively. Transduction of dn-Akt inhibits Ach-induced vascular relaxations (
c), whereas SNP-induced relaxations are not affected (
d). Data are presented as mean ± SEM. (
n = 9 rings for β-gal–transduced and 10 rings for dn-Akt–transduced vessels isolated from four mice.
AP < 0.05 relative to the β-gal–transduced vessels by ANOVA.)
