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. Author manuscript; available in PMC: 2022 Dec 27.
Published in final edited form as: Br J Pharmacol. 2021 Aug 7;178(20):4119–4136. doi: 10.1111/bph.15602

Figure 6.

Figure 6.

The PKG inhibitor, 15 μM Rp-8-Br-PET-cGMPS blocked contractions and dilations of WT and Kir6.1−/− vessels to increasing concentrations of NONOate. Representative traces of NONOate concentration-dependent responses after pre-incubation with 15 μM Rp-8-Br-PET-cGMPS in WT (A) and Kir6.1−/− (B) popliteal lymphatics. Comparisons of contraction amplitude (C) and frequency (D) before (“Krebs”) and after treatment of Rp-8-Br-PET-cGMPS, * Significant using paired Student’s t-test). Lymphatic contraction parameters were normalized to their respective values before Rp-8-Br-PET-cGMPS treatment (E-G). The effect of NONOate on normalized amplitude (E), normalized frequency (F) and change in EDD (G) in the presence of 15 μM Rp-8-Br-PET-cGMPS. Filled red rectangles indicate NONOate responses of WT vessels pretreated with Rp-8-Br-PET-cGMPS (n=10) and open blue rectangles represent NONOate responses of Kir6.1−/− pretreated with Rp-8-Br-PET-cGMPS (n=11). For comparison, the responses to NONOate only in each group of WT (n=24) and Kir6.1−/− (n=9) are represented by filled black circles and open black rectangles respectively. All data are means ± SEM. * Significant difference in WT data from control (absence of NONOate). † Significant difference in Kir6.1−/− data from control (absence of NONOate). ¥ (red) Significant difference between filled black circle and filled red rectangle data points. € (blue) Significant difference between open black circle and open blue rectangle data points (P < 0.05).