Impairment of endothelium-dependent relaxation of rabbit aortas by cigarette smoke extract—role of free radicals and attenuation by captopril

Ota, Yasutaka; Kugiyama, Kiyotaka; Sugiyama, Seigo; Ohgushi, Masamichi; Matsumura, Toshiyuki; Doi, Hideki; Ogata, Nobuhiko; Oka, Hideki; Yasue, Hirofumi

doi:10.1016/s0021-9150(97)06106-6

Cited by 141 publications

(95 citation statements)

References 34 publications

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“…Our findings in regard to the direct actions of CSE on NOS enzymatic activity are consistent with studies that predict that the catalytic domain of human eNOS contains 10 cysteine residues with 2 of them (Cys-94 and Cys-99) being responsible for coordinating an intermolecular interaction between 2 monomers. 35 Although our observations are also consistent with previous reports, 13,[22][23][24] some longer-term studies 13,[22][23][24] suggest that a reduction in NOS activity parallels to some extent a decrease in eNOS content. In our study, we saw a more rapid onset of the inhibitory effect of CSE on NOS activity, using isolated purified eNOS enzyme.…”

Section: Discussionsupporting

confidence: 89%

“…Previous studies suggest that the effect of CSE may relate in part because of reduced NOS expression and enzymatic activity. 13,[22][23][24] Alternatively, Hutchison et al 5 showed previously that arginine supplementation attenuated the endothelial dysfunction caused by exposure to cigarette smoke, suggesting that substrate availability for NOS may be a key mechanism for CSE-induced endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

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Adverse Effects of Cigarette Smoke on NO Bioavailability

et al. 2006

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Abstract-Endothelial dysfunction is a hallmark of cardiovascular disease, and the L-arginine:NO pathway plays a critical role in determining endothelial function. Recent studies suggest that smoking, a well-recognized risk factor for vascular disease, may interfere with L-arginine and NO metabolism; however, this remains poorly characterized. Accordingly, we performed a series of complementary in vivo and in vitro studies to elucidate the mechanism by which cigarette smoke adversely affects endothelial function. In current smokers, plasma levels of asymmetrical dimethyl-arginine (ADMA) were 80% higher (Pϭ0.01) than nonsmokers, whereas citrulline (17%; PϽ0.05) and N-hydroxy-L-arginine (34%; PϽ0.05) were significantly lower. Exposure to 10% cigarette smoke extract (CSE) significantly affected endothelial arginine metabolism with reductions in the intracellular content of citrulline (81%), N-hydroxy-L-arginine (57%), and arginine (23%), while increasing ADMA (129%). CSE significantly inhibited (38%) arginine uptake in conjunction with a 34% reduction in expression of the arginine transporter, CAT1. In conjunction with these studies, CSE significantly reduced the activity of eNOS and NO production by endothelial cells, while stimulating the production of reactive oxygen species. In conclusion, cigarette smoke adversely affects the endothelial L-arginine NO synthase pathway, resulting in reducing NO production and elevated oxidative stress. In conjunction, exposure to cigarette smoke increases ADMA concentration, the latter being a risk factor for cardiovascular disease. Key Words: smoking Ⅲ endothelium Ⅲ metabolism A therosclerotic coronary and cerebrovascular disease are leading causes of death and disability in the Western world, and cigarette smoking has been clearly identified as a risk factor for coronary artery disease (reviewed by Ambrose and Barua 1 ). In this context, measures of endothelial function have been associated with cardiovascular outcome, 2 and smoking has been widely associated with reduced endothelial function. 3 The endothelium plays a central role in the modulation of vascular tone, the inhibition of platelet aggregation and vascular smooth muscle proliferation, and a key participation in angiogenesis under appropriate conditions. NO is well recognized as playing a pivotal part in these endothelial properties, being produced by the endothelial isoform of NO from its preferred substrate L-arginine. In this context, provision of sufficient L-arginine is critical for the sustained production of NO supply, 4 mediated in endothelial cells (ECs) principally by the type 1 cationic amino acid transporter (CAT1). Previous studies indicate that deleterious actions of cigarette smoke on endothelial function could be mitigated by supplemental L-arginine; 5 however, to date, the precise basis for this interaction remains unclear. One explanation is that cigarette smoke exerts an inhibitory effect on components of the L-arginine:NO pathway to influence NO production. In addition, potential effects of cigar...

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Adverse Effects of Cigarette Smoke on NO Bioavailability

et al. 2006

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2010

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Although cigarette smoking is known to be an important risk factor for renal disease, the mechanism by which smoking induces progressive renal disease in a healthy population has not been established. We hypothesized that oxidative stress (measured as 8-iso-prostaglandin F 2a , 8-iso-PGF2a), inflammation (highly sensitive C-reactive protein (CRP), hs-CRP) and nitric oxide may be associated with an alteration in the estimated glomerular filtration rate (eGFR) and proteinuria in otherwise healthy smokers. A total of 649 eligible subjects were classified according to their smoking status. Plasma NOx was measured using ozone-based chemiluminescence, urinary 8-iso-PGF2a was measured using enzyme immunoassay and serum hs-CRP was measured using a latex aggregation nephelometry method. The levels of 8-iso-PGF2a and hs-CRP increased in current smokers (P¼0.001 and P¼0.029, respectively), although there was not an increase in the NOx level. The prevalence of a high eGFR increased in light smokers (odds ratio (OR) 1.15 (95% confidence interval (CI), 0.61-2.17)) and heavy smokers (OR 2.33 (95% CI, 1.06-5.10)) when compared with non-and past smokers (P for trend¼0.024). The multivariable-adjusted mean values of the eGFR in current smokers, reported from the lowest to the highest quintiles of hs-CRP levels, were 82.1, 85.1, 86.4 and 88.5 ml per min per 1.73 m 2 (P for trend¼0.027). The mean values of proteinuria were 28.6, 34.6, 37.2 and 39.5 mg g À1 creatinine (P for trend¼0.003). The correlation coefficient between hs-CRP and eGFR was increased significantly (P¼0.03) across non-(r¼0.03), past (r¼À0.17), light (r¼0.13) and heavy smokers (r¼0.31). In conclusion, cigarette smoking is a risk factor for renal function alteration in healthy smokers and is characterized by a high eGFR and a high urinary protein associated with an increase in the hs-CRP. This finding suggests that hs-CRP may help mediate the alteration of renal function in smokers.

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“…32 It is reported that secondhand smoking impairs endothelium-dependent relaxation of isolated rabbit arteries and the impaired relaxations of arteries mediated through the degradation of released NO by superoxide anion derived from cigarette smoke. 9,33,34 Therefore, it is speculated that secondhand smoking-induced impaired neurogenic and endotheliumdependent relaxation may be due to the increase in oxygen-derived free radicals production in smoke, as reported by Ota et al, 33 which may inactivate NO continuously released from endothelial cells.…”

Section: Discussionmentioning

confidence: 95%

Secondhand tobacco smoke impairs neurogenic and endothelium-dependent relaxation of rabbit corpus cavernosum smooth muscle: improvement with chronic oral administration of L-arginine

et al. 2005

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The first goal of this study was to examine the effect of secondhand smoking on neurogenic, endothelium-and cGMP-dependent relaxant responses of rabbit corpus cavernosum smooth muscle. Our second goal was to determine whether such an effect can be prevented by oral administration of L-arginine. Male New Zealand rabbits were divided into control, chronic passive cigarette smoking and L-arginine treatment groups. Relaxant or contractile responses in isolated corpus cavernosum smooth muscle strips were determined by using in vitro muscle technique. There was no significant difference in the relaxant response of the strips to papaverine, sodium nitroprusside and contractile response to KCl among the groups. Relaxant responses to acetylcholine and electrical field stimulation and contractile response to phenylephrine were significantly decreased in the strips of the smoking group than that of the control group. The impaired relaxations of strips were markedly improved by treatment of L-arginine, but the contractile responses to phenylephrine were not affected. These data indicate that secondhand smoking may impair both neurogenic and endothelium-dependent relaxation of corpus cavernosum smooth muscle, and may contribute to the etiology of impotence. Chronic dietary supplementation with L-arginine offsets the impairment of neurogenic and endothelial relaxation. Therefore, we suggest that secondhand smoking exposure to cigarette produces selective impairment of neurogenic and endothelium-dependent relaxation of corpus cavernosum smooth muscle via a mechanism related to the decreased production and/or availability of nitric oxide.

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Impairment of endothelium-dependent relaxation of rabbit aortas by cigarette smoke extract—role of free radicals and attenuation by captopril

Cited by 141 publications

References 34 publications

Adverse Effects of Cigarette Smoke on NO Bioavailability

Adverse Effects of Cigarette Smoke on NO Bioavailability

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

Secondhand tobacco smoke impairs neurogenic and endothelium-dependent relaxation of rabbit corpus cavernosum smooth muscle: improvement with chronic oral administration of L-arginine

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