Effects of Hyperglycemia on Vascular Smooth Muscle Ca²⁺ Signaling

Figure 9

Ca²⁺ signaling pathways in normal (NHVSMC) and diabetic (DHVSMC) human aortic VSM cells. Cells were loaded with 2 μM Fura-2AM for 30 min and passive leak was monitored after store depletion with 1 μM thapsigargin (TG). Peak amplitude in response to TG (TG max release) and the time to half maximum release were compared between normal and diabetic cells (a, b). For the extrusion pathways the activity of PMCA and NCX was monitored by Ca²⁺ imaging after store depletion with 1 μM TG. Time to half () decay was then measured and compared between the different conditions (c). Cells were labeled with 2 μM Fura-2AM for 30 min and Ca²⁺ release was imaged following treatment of the cells with 30 and 40 μM of PE (d) or by using 30 μM PE followed by 1 mM lanthanum chloride (La³⁺) (e). Time to half decay was then measured and compared between normal and diabetics cells (e). Data are presented as mean ± SE from at least three independent experiments done each in triplicate. ; NS: not significant.

(a)

(b)

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(e)