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. Author manuscript; available in PMC: 2012 Sep 2.
Published in final edited form as: Free Radic Biol Med. 2011 Oct 7;52(2):427–435. doi: 10.1016/j.freeradbiomed.2011.09.020

Fig. 2.

Fig. 2

PI3K involvement in GTN-dependent vasodilation. (A) Effect of wortmannin (PI3K inhibitor) pretreatment upon the acetylcholine (Ach)- or GTN-induced dilation of rat aortic rings. (B) Nitroglycerin EC50 values measured in rat aortic rings in the presence of the indicated concentrations of Akt 1/2 inhibitor. (C) Vasodilation experiment with mesenteric tissue recovered from p110γ-knockout mice. p110γ is the catalytic subunit of endothelial PI3K enzyme. Both pharmacologic inhibition and genetic knockout of PI3K inhibited GTN-induced dilation of conducing (aorta) and resistant (mesenteric artery) vessels. *P<0.05, **P<0.01.