TY - GEN
T1 - Biochemical verification of smoking cessation and the role of endothelin‐1
T2 - Impact on cardiovascular disease risk
AU - Tingen, Martha S
AU - Sojourner, Samantha J
AU - Tucker, Matthew A
AU - Derella, Cassandra C
AU - Harris, Ryan A
PY - 2019/4/1
Y1 - 2019/4/1
N2 - Smoking is an independent risk factor for cardiovascular disease (CVD). Endothelin‐1 (ET‐1), a potent vasoconstrictor peptide that also increases CVD risk, is transiently elevated following smoke exposure and is associated with self‐reported smoking status. Whether biochemical verification (i.e. serum cotinine) of smoking cessation over time is associated with changes in circulating ET‐1 has yet to be determined. To examine the impact of smoking cessation on the relationship between cotinine and ET‐1 over time. 35 individuals (aged 36 ± 10 yr., BMI 28.0 ± 5.7 kg/m2), participated in a 3‐month smoking cessation program. Measurements of resting systolic and diastolic blood pressures (SBP and DBP), serum cotinine, and plasma ET‐1 were determined at baseline, and immediately (3 months) and long‐term (12 months) following the smoking cessation program. Serum cotinine, a prominent metabolite of nicotine, was measured using liquid chromatography with mass‐spectrometric detection and plasma ET‐1 via microfluidic colorimetric assay. A significant reduction was observed in serum cotinine from baseline to immediately (3 months) following smoking cessation (176.1 ± 122.5 ng/ml vs. 53.0 ± 91.2 ng/ml, p<0.001) and persisted out to 12 months (84.8 ± 96.9 ng/ml, p<0.001). Similarly, plasma ET‐1 was significantly lower at 3 months (1.84 ± 0.60 pg/ml, p = 0.003) and at 12 months (1.93 ± 0.80 pg/ml, p = 0.018) following smoking cessation compared with baseline (2.18 ± 0.66 pg/ml). A significant association was observed between baseline levels of cotinine and ET‐1 (r = 0.369, p = 0.029). Additionally, the change in cotinine at 12 months following smoking cessation was associated (r = 0.402, p = 0.034) with the change in ET‐1 at 12 months. Although not statistically significant, clinically meaningful reductions in SBP (−2.0 ± 2.4 mm Hg, p = 0.406) and DBP (−3.6 ± 1.9 mm Hg, p = 0.062) were observed at 3 months following smoking cessation. Using biochemical verification of smoking status in smokers, the present study identified a relationship between serum cotinine and circulating ET‐1. The 3‐month smoking cessation program not only lowered serum cotinine, but also reduced circulating concentrations of ET‐1 and blood pressure. In fact, at 12 months following smoking cessation, the change in serum cotinine was significantly associated with the change in ET‐1. The long‐term improvement of CVD risk with smoking cessation may be in part through a reduction in circulating ET‐1; however, future studies are warranted to test this hypothesis. Support or Funding Information Funding Provided by the Georgia Cancer Center This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
AB - Smoking is an independent risk factor for cardiovascular disease (CVD). Endothelin‐1 (ET‐1), a potent vasoconstrictor peptide that also increases CVD risk, is transiently elevated following smoke exposure and is associated with self‐reported smoking status. Whether biochemical verification (i.e. serum cotinine) of smoking cessation over time is associated with changes in circulating ET‐1 has yet to be determined. To examine the impact of smoking cessation on the relationship between cotinine and ET‐1 over time. 35 individuals (aged 36 ± 10 yr., BMI 28.0 ± 5.7 kg/m2), participated in a 3‐month smoking cessation program. Measurements of resting systolic and diastolic blood pressures (SBP and DBP), serum cotinine, and plasma ET‐1 were determined at baseline, and immediately (3 months) and long‐term (12 months) following the smoking cessation program. Serum cotinine, a prominent metabolite of nicotine, was measured using liquid chromatography with mass‐spectrometric detection and plasma ET‐1 via microfluidic colorimetric assay. A significant reduction was observed in serum cotinine from baseline to immediately (3 months) following smoking cessation (176.1 ± 122.5 ng/ml vs. 53.0 ± 91.2 ng/ml, p<0.001) and persisted out to 12 months (84.8 ± 96.9 ng/ml, p<0.001). Similarly, plasma ET‐1 was significantly lower at 3 months (1.84 ± 0.60 pg/ml, p = 0.003) and at 12 months (1.93 ± 0.80 pg/ml, p = 0.018) following smoking cessation compared with baseline (2.18 ± 0.66 pg/ml). A significant association was observed between baseline levels of cotinine and ET‐1 (r = 0.369, p = 0.029). Additionally, the change in cotinine at 12 months following smoking cessation was associated (r = 0.402, p = 0.034) with the change in ET‐1 at 12 months. Although not statistically significant, clinically meaningful reductions in SBP (−2.0 ± 2.4 mm Hg, p = 0.406) and DBP (−3.6 ± 1.9 mm Hg, p = 0.062) were observed at 3 months following smoking cessation. Using biochemical verification of smoking status in smokers, the present study identified a relationship between serum cotinine and circulating ET‐1. The 3‐month smoking cessation program not only lowered serum cotinine, but also reduced circulating concentrations of ET‐1 and blood pressure. In fact, at 12 months following smoking cessation, the change in serum cotinine was significantly associated with the change in ET‐1. The long‐term improvement of CVD risk with smoking cessation may be in part through a reduction in circulating ET‐1; however, future studies are warranted to test this hypothesis. Support or Funding Information Funding Provided by the Georgia Cancer Center This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
M3 - Article
SN - 0892-6638
VL - 33
JO - FASEB Journal
JF - FASEB Journal
ER -
