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. 2019 Feb 7;23(4):2801–2812. doi: 10.1111/jcmm.14188

Figure 3.

Figure 3

Pretreatment with L‐NAME reduces LMK235‐mediated vasorelaxation in rat mesenteric arteries as well as LMK235‐induced nitric oxide production in HUVECs. (A) LMK235 was added cumulatively to elicit relaxation when vascular contraction induced by U46619 (30 nmol/L) reached plateaus in endothelium‐intact (open circle) or endothelium‐denuded (black circle) rat aortic rings. Relaxation is expressed as a percentage of the maximal contraction. Data are expressed as mean ± SEM. *P < 0.05 and **P < 0.01 vs endothelium intact at the same concentration points of LMK235. (B) Mesenteric artery rings were pretreated with L‐NAME (100 μmol/L) or vehicle (0.1% dimethylsulphoxide) for 30 min. LMK235 or vehicle was added cumulatively to elicit relaxation when vascular contractions in rat mesenteric arteries induced by U46619 reached a plateau (n = 4). Data are expressed as mean ± SEM. ***P < 0.001 vs vehicle‐treated group; ## P < 0.01 vs vehicle‐treated LMK235 group at the same concentration points of LMK235. (C) HUVECs were treated with LMK235 (1 μmol/L) in the presence or absence of L‐NAME (250 μmol/L) for 24 h and labelled with a fluorescent nitric oxide indicator, DAF‐FM DA (2.5 μmol/L), for 30 min. Three independent experiments were conducted, and representative images are shown. Scale bar = 100 μm