Affiliation:
1. Department of Health and Human Physiology, The University of Iowa, Iowa City, IA (K.M.H., E.M.W., A.E.S.).
2. Department of Internal Medicine, Carver College of Medicine, Iowa City, IA (J.L.C.).
Abstract
BACKGROUND:
Chronic electronic-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.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Cited by
4 articles.
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