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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Hypertension. 2014 Oct 13;65(1):130–139. doi: 10.1161/HYPERTENSIONAHA.114.04473

Figure 6.

Figure 6

(A) Cumulative concentration-response curves to diamide and(DTT) in MAs derived from wt mice. (B) DTT reverses diamide-induced inhibition of PHE-induced increase in active tension. Representative tracing showing tension changes in a MAs isolated from a wt mouse contracted with PHE before, during and after application of diamide, followed by addition of DTT. (C) EDH responses (in the presence of L-NAME and INDO in MAs derived from wt mice treated without (CON, open circles), 0.1 μmol/L diamide (open diamonds) or 1 μmol/L diamide (closed diamonds). Insert: Effect of IK1 channel inhibition by TRAM-34 on the EDH responses. (D) EDH responses in MAs derived from wt mice treated without (CON, open squares), 0.1 μmol/L DTT (open squares), or 1 μmol/L DTT (closed squares). Insert: Effect of IK1 channel inhibition by TRAM-34 on the EDH responses. (E) EDH responses in MAs derived from wt mice treated with 0.3 μmol/L diamide in the additional presence of either 0.1 μmol/L DTT (circles), 1 μmol/L DTT (squares) or 10 μmol/L DTT (diamonds). (F) MAs derived from dnTrx-Tg (downward triangles) mice were treated for 30 min with either vehicle (H2O; CON) or = DTT and were assessed for endothelium-dependent relaxations to cumulative concentrations of ACh =. Values are means ± SEM (n=4–6 mice). * P< 0.05.