Figure 3.

Data showing the temporal response of maximal [10⁻⁴] ACh-stimulated middle cerebral artery (MCA) incubated with (A) L-NAME, a nitric oxide (NO) inhibitor, or (B) TEMPOL, a superoxide dismutase mimetic (i.e. scavenger for superoxide anion). In (A), data show the inhibition of NO production in Air (control) animals results in ~50% impairment in MCA reactivity. Similar degree of impairment (i.e. ~50%) is observed in Ecig and 3R4F Cigarette exposed animals on D0 and D1, with or without L-NAME, suggesting the impairment is mostly attributable to reduced NO bioavailability. Partial recovery of the MCA reactivity (for both Ecig and 3R4F) begins by D2, and is fully recovered by D3, but again, is lost in the presence of L-NAME, further supporting the importance of altered NO underpinning the vascular impairment observed in response to Ecig and 3R4F on D0, D1 and D2. In (B), data show TEMPOL has small effect by improving MCA reactivity on D0, and then fully restores MCA dilation response on D1-3. In contrast, TEMPOL does not rescue the impaired reactivity in 3R4F Cigarette exposed animals, suggesting that superoxide-induced ROS activity plays a role with vascular dysfunction associated with Ecigs but not cigarettes.