Skip to main content
. 2012 Aug;166(7):2024–2035. doi: 10.1111/j.1476-5381.2012.01832.x

Figure 3.

Figure 3

PI3K and Akt participate in renin-mediated eNOS-Ser1177 phosphorylation in the NTS. (A) The quantitative immunoblotting analysis demonstrates that renin treatment increased the level of P-Akt-Ser473 protein in the NTS. Densitometric analysis of P-Akt-Ser473 protein levels (means ± SEM, n= 6) after administration of aCSF or renin. *P < 0.05, significantly different from the aCSF group. (B) Representative tracings reveal the effects of BP by microinjection renin (240 fg) into the NTS pretreated with Akt inhibitor, Akt inhibitor IV (375 fmol). *P < 0.05, significantly different from the renin group. (C) The blood pressure of renin (240 fg) injection into the NTS after administration of the PI3K inhibitor, LY294002 (6 pmol). Representative tracings demonstrate that the depressor effect of renin was significantly attenuated by LY294002. Summary data (means ± SEM, n= 6) are shown in the graph. *P < 0.05, significantly different from the renin group. (D) Immunoblotting analysis reveals that the P-eNOS-Ser1177 protein level was increased after renin administration in the NTS. Phosphorylation of eNOS-Ser1177 was reduced by pretreatment with LY294002. Densitometric analysis of P-eNOS-Ser1177 protein levels (means ± SEM, n= 6) after treatment with aCSF, renin or LY294002. *P < 0.05, significantly different from the aCSF group; #P < 0.05, significantly different from the renin group.