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. 2016 Dec 26;595(7):2339–2364. doi: 10.1113/JP273255

Figure 7. Loss of Kir2.1 function with dominant negative Kir2.1 results in the inhibition of FIV in mesenteric arteries.

Figure 7

A, representative whole‐cell Kir current traces elicited by linear voltage ramps recorded from human aortic endothelial cells with dnKir2.1 and empty lentiviral constructs. Shown are average Kir current densities in human aortic endothelial cells with dnKir2.1 and empty lentiviral constructs at −90 mV (empty, n = 13 in 3 independent experiments; dnKir2.1, n = 9 in 2 independent experiments; * P < 0.05). B, dnKir2.1 or empty lentiviral constructs were intraluminally applied to intact mesenteric arteries for 24 h. Shown are average flow‐induced dilatation of pre‐constricted lentiviral constructs‐treated and non‐treated mesenteric arteries harvested from WT mice, as a function of pressure gradient. Vessel diameters are normalized to diameters stabilized at 60 cmH2O and the intraluminal pressure was maintained at the same pressure. Ba2+ (300 μm) was perfused extravascularly on to WT mesenteric arteries without the transfection of lentiviral constructs (n = 3 per group, * P < 0.05). C, average dilatations at Δ100 cmH2O.