Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries

Abstract

Cigarette smoking (CS) is a major risk factor for vascular disease. The aim of this study was to quantitatively assess the influence of CS on mouse arteries. We studied the effect of short-term (6 wk) and long-term (16 wk) CS exposure on structural and mechanical properties of coronary arteries compared with that of control mice. We also examined the reversibility of the deleterious effects of CS on structural [e.g., wall thickness (WT)], mechanical (e.g., stiffness), and biochemical [e.g., nitric oxide (NO) by-products] properties with the cessation of CS. The left and right coronary arteries were cannulated in situ and mechanically distended. The stress, strain, elastic modulus, and WT of coronary arteries were determined. Western blot analysis was used to analyze endothelial NO synthase (eNOS) in the femoral and carotid arteries of the same mice, and NO by-products were determined by measuring the levels of nitrite. Our results show that the mean arterial pressure was increased by CS. Furthermore, CS significantly increased the elastic modulus, decreased stress and strain, and increased the WT and WT-to-radius ratio compared with those of control mice. The reduction of eNOS protein expression was found only after long-term CS exposure. Moreover, the NO metabolite was markedly decreased in CS mice after short- and long-term exposure of CS. These findings suggest that 16 wk of CS exposure can cause an irreversible deterioration of structural and elastic properties of mouse coronary arteries. The decrease in endothelium-derived NO in CS mice was seen to significantly correlate with the remodeling of arterial wall.

C-reactive protein is associated with cigarette smoking-induced hyperfiltration and proteinuria in an apparently healthy population

“…42 Moreover, Barua et al 40 and Rångemark and Wennmalm 43 reported no differences in the NOx level among smoking groups, which is similar to our findings. 39,43 Cigarette smoking generates O 2 ÁÀ which contributes to the catalysis of arachidonic acid peroxidation to F 2 -isoprostanes, leading to a high level of F 2 -isoprostanes in smokers, as shown in this study and other studies. 44, 45 We did not find a correlation between 8-iso-PGF2a and either the eGFR or urinary protein in apparently healthy smokers.…”

“…In vitro and in vivo studies showed a reduction of NO after cigarette smoking exposure. [37][38][39] However, the majority of in vitro data has involved the use of cigarette smoke extract solution, which is probably not an appropriate physiological model, as circulating particulate of cigarette smoke has to first bypass the lung. 40 Thus, the effect of smoking on the NO pathway seems to be more complex on a cellular level than suggested by the described Abbreviations: ALT, alanine transaminase; ANOVA, analysis of variance; AST, aspartate aminotransferase; BMI, body mass index; BP, blood pressure; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; g-GTP, g-glutamyl transpeptidase; HbA1c, hemoglobin A1c; HDL-c, high-density lipoprotein-cholesterol; HOMA, homeostatic model assessment; LDL-c, low-density lipoprotein-cholesterol; NS, nonsignificant.…”

Improvement in blood pressure after short-term inorganic nitrate supplementation is attenuated in cigarette smokers compared to non-smoking controls

“…This suggests that the bioavailability of NO 2 --derived NO, and the accompanying lowering of blood pressure, might be compromised in smokers at a given NO 3 -dose. Moreover, cigarette smoking is associated with heightened inflammatory, oxidative and nitrative stress, which contributes to vascular remodelling and biochemical dysfunction [72][73][74]. These negative effects on the vasculature might lower the responsiveness of the blood vessels to dilate at a given plasma [NO 2 -] which could account for our findings of improved blood pressure in non-smokers, but not smokers, after short-term dietary NO 3 -supplementation.…”

Akciğerde Rhoa/Rho-Kinaz Sinyalizasyon Yolu Üzerine Sigara İçmenin Etkisi

“…In addition, it reduces Larginine transport and nitric oxide synthase expression and activity (6). Long-term cigarette smoke exposure irreversibly disrupts the mouse carotid artery structure and reduces the elasticity thereof (7). Smoking increases the risk of chronic obstructive pulmonary disease.…”