In:
Hypertension, Ovid Technologies (Wolters Kluwer Health)
Abstract:
Chronic e-cigarette (EC) use is reported to decrease vascular endothelial function. However, the mechanism(s) mediating this reduction remain unclear. In this study, we examined endothelium- and NO-dependent dilation, and the role of oxidative stress in attenuating these responses, in healthy young EC users (n=20, 10 males/10 females) compared with healthy controls (n=20, 10 males/10 females). We hypothesized that EC would have reduced endothelium- and NO-dependent dilation and administration of the superoxide scavenger tempol would increase these responses in EC. We further hypothesized that female EC would have the greatest reductions in endothelium- and NO-dependent dilation. Methods: We assessed microvascular endothelium-dependent vasodilator function in vivo by measurement of cutaneous vascular conductance (%CVCmax) responses to a standardized local heating protocol in control and 10 μM tempol-treated sites. After full expression of the local heating response, 15 mM N G -nitro-L-arginine methyl ester (NO synthase inhibition) was perfused. Results: EC had significantly reduced endothelium- (73±15 versus 87±9%CVCmax; P 〈 0.001) and NO-dependent (48±17% versus 62±15%; P =0.011) dilation. Tempol perfusion increased endothelium-dependent (84±12%CVCmax P =0.01) and NO-dependent (63±14% P =0.005) dilation in EC but had no effect in healthy control. Within female sex, EC had lower endothelium-dependent (71±13 versus 89±7%CVCmax; P =0.002) and NO-dependent (50±6 versus 69±11%; P =0.005) dilation compared with healthy control, and tempol augmented endothelium-dependent (83±13%CVCmax; P =0.002) and NO-dependent (62±13%; P =0.015) dilation. There were no group or treatment differences within male sex. Conclusion: Healthy young adult EC users have reduced microvascular endothelium-dependent and NO-dependent dilation, driven by greater reductions in female EC users, and mediated in part by superoxide.
Type of Medium:
Online Resource
ISSN:
0194-911X
,
1524-4563
DOI:
10.1161/HYPERTENSIONAHA.123.21684
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2023
detail.hit.zdb_id:
2094210-2
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