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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: J Hypertens. 2013 Feb;31(2):303–311. doi: 10.1097/HJH.0b013e32835bbb83

Figure 3. Insulin activates NCC cotransporter through a PI3K-mTORC2-AKT pathway.

Figure 3

Xenopus laevis oocytes were injected with rNCC cRNA and three days later Na+ uptake was assessed by incubated the oocytes in the absence (white bars) or presence (black bars) of insulin, in the absence or presence of the PI3K inhibitor wortmannin (A), the specific inhibitor of mTORc2, AZD8055 (B); or in the presence of the AKT Inhibitor, AKT IV-I (C). or the inhibitors of MAP kinases. The mean value of the cotransporter without insulin was taken as 1 and the effect of insulin was normalized to that value (*p<0.0001 vs own control in the absence of insulin). (D) NCC activity was analyzed in mDCT15 cells in the in the absence (white bars) or presence of 20 U/ml insulin (black bars) with or without wortmannin or the AKT inhibitor (*p<0.01 vs control).