Figure 1.

Dyslipidemia reduces shear stress–induced increases in endothelial cell (EC) inwardly rectifying K⁺ (Kir) current without influencing Kir2.1 channel expression in vitro. Representative traces of Kir currents from (A) control and (B) acetylated low‐density lipoprotein (acLDL; 50 μg/mL [24 hours])–treated mesenteric endothelial cells. Ramps from −120 to +40 mV elicited inward K⁺ currents that reversed around −21 mV. Insets represent the increase in current (I_{Δ SS}) evoked by 0.7 dynes/cm² in the respective traces. Shear significantly increased Kir current in (C) control (n=8) and (D) acLDL‐treated (n=7) ECs. Treating ECs with acLDL inhibited (E) baseline Kir currents recorded in a static bath (n=9 and 10 cells for control and acLDL, respectively) and (F) the shear‐induced increase in Kir current. For (E and F), a paired or unpaired Student t test was used where appropriate. Cell capacitance was similar between control and acLDL‐treated ECs (10.0±1.7 pF vs 11.8±1.5 pF, respectively). Note that Kir channel protein expression was not altered by treatment with acLDL in (G) a representative blot and (H) group data (n=5) normalized to the loading control, GAPDH. For accurate comparison of densitometry from separate blots, control samples were first normalized to 1. An unpaired Student t test was used to test for significant differences. For all group data, error bars represent SEM. *P<0.05.