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Secondhand smoke exposure impairs vascular reactivity in mesenteric arteries
Author(s) -
NievesCintron Madeline,
Syed Arsalan,
Pan Shiyue,
Karey Emma,
Sun Junqing,
Navedo Manuel,
Chen ChaoYin
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.770.14
Subject(s) - mesenteric arteries , vasoconstriction , vasodilation , medicine , vascular smooth muscle , endocrinology , cardiology , anatomy , smooth muscle , artery
Secondhand smoke (SHS) has significant detrimental vascular effects, including enhanced vasoconstriction and hypertension. Yet, the mechanisms linking SHS exposure to these complications are unclear. Although the multifactorial nature of these changes is well appreciated (e.g. endothelial dysfunction, aberrant central control regulation), impaired vascular smooth muscle (VSM) function may also be a key, yet poorly explored, contributing factor. In this study, we tested the hypothesis that vascular reactivity of small diameter mesenteric arteries is altered in mice exposed to SHS. Mice were randomized into control (filter air, FA) and experimental (SHS) groups and exposed to either FA or SHS (Total Suspended Particle, TSP = 3 ± 1 mg/m 3 ; 6 hrs/day, 5 days/week) for a 12 weeks period. After 12 weeks, mesenteric arteries from mice exposed to SHS showed higher (P < 0.05) myogenic tone compared to arteries from the FA group (15.7 ± 2 vs. 23.2 ± 2 FA vs. SHS, respectively). Moreover, we found reduced ACh‐induced vasodilation in SHS arteries (p < 0.05). Consistent with elevated myogenic tone, the resting membrane potential (V m ) of VSM cells isolated from mesenteric arteries of mice exposed to SHS was more depolarized (p < 0.05) than in cells from arteries from the FA group (−42.3 ± 3 vs. −35 ± 2, FA vs. SHS, respectively). Our next series of experiments will examine mechanisms mediating changes in V m in VSM from SHS versus FA. Our results suggest that SHS have deleterious effects on the vasculature that may involve changes in VSM function. Support or Funding Information This work was supported by NIH R01ES025229, R01HL098200, R01HL121059, and NIH‐T32 HL086350. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .