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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 2.

Figure 2

(A) Depolarization (60 mmol/L K+ KRB)-induced, and (B) induced contraction in MAs derived from wt (white bars), Trx-Tg (blue bars) and dnTrx-Tg (red bars) mice. MAs derived from wild-type (circles), Trx-Tg (upward triangles) and dnTrx-Tg (downward triangles) mice were assessed for: (C) Endothelium-dependent relaxations to cumulative concentrations of ACh. (D) Endothelium-independent relaxations in MAs pretreated with L-NAME and indomethacin (INDO) contracted with a submaximal concentration of PHE, and assessed with cumulative concentrations of SNP. (E) NO-mediated endothelium-dependent relaxations in MAs pretreated for 30 min with INDO the IK1 channel blocker TRAM-34 and the SK3 channel blocker UCL-1684, to block EDH-mediated responses, contracted with PHE before assessing relaxing responses to cumulative concentrations of ACh. (F) Endothelium-dependent hyperpolarizing (EDH) responses in MAs treated with the NO synthase blocker L-NAME and INDO followed by cumulative concentrations of ACh. Values are means ± SEM (n=8–10 mice). * P< 0.05 Trx-Tg compared with wt, # P< 0.05 dnTrx-Tg compared with wtand Trx-Tg, ** P< 0.05 Trx-Tg compared with wtand dnTrx-Tg.