Ascorbic Acid Prevents Cigarette Smoke Injury to Endothelium-Dependent Arterial Relaxation

Mays, Bradley W.; Freischlag, Julie A.; Eginton, Mark T.; Cambria, Robert A.; Seabrook, Gary R.; Towne, Jonathan B.

doi:10.1006/jsre.1999.5601

Cited by 32 publications

(16 citation statements)

References 28 publications

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“…Endothelial cell function is impaired in patients with atherosclerosis and could antecede the development of overt evidence of the disease. Cigarette smoke augments leucocyte-endothelial interactions, thought to be relevant to the early stages of atherogenesis ex vivo and in vitro, 80,81 and this effect is neutralized by vitamin C. 81 Congruently, endothelial cell function is also impaired by passive exposure to cigarette smoke 82 and in apparently healthy chronic smokers, in whom the defect is largely corrected with vitamin C. 83 Interestingly, vitamin C, but not vitamin E, depresses elevated urinary iPs in smokers. 75 Exposure to secondhand smoke also impairs acutely coronary endothelial function, 84 and acute smoking is associated with a rapid depletion of endogenous nitrate and nitrite, reflecting NO · generation and endogenous antioxidants.…”

Section: Ros and Vascular Disease: Human Studiesmentioning

confidence: 99%

Oxidative Stress and Cardiovascular Injury

2003

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T his review so far has considered the role of vascular cells in the generation of reactive oxygen species (ROS) and novel approaches to their detection in integrated systems such as animal models of vascular disease and humans. We now turn attention to evidence consistent with a role for ROS in models of human disease and in discrete patient populations. We also briefly comment on the outcomes of clinical trials of antioxidants. Mainly, these have been disappointing. However, it is premature to conclude that the oxidation hypothesis of disease causality has been adequately tested. ROS and Vascular Disease: Animal StudiesAnimal studies, for the most part, support a fundamental role for ROS in cardiovascular disease. Any controversy could in part reflect the use of ineffective antioxidants and the selection of models in which ROS generation is of marginal relevance to the measured outcome. Both of these issues require a quantitatively accurate measurement of drug effect (ie, antioxidant capacity) before hypotheses relating to the role of oxidant stress can be addressed rationally. These issues pertain to clinical trials also, as we will discuss. However, animal studies permit administration of much more powerful antioxidants (eg, rate constant for interaction of superoxide dismutase (SOD) with O 2 ·Ϫ Ϸ1.6ϫ10 9 · mol/L Ϫ1 · s Ϫ1 ) than is possible in humans (eg, rate constant for vitamin E Ϸ0.59 mol/L Ϫ1 · s Ϫ1 ) or, like in the case of vitamin E, doses of the antioxidant in excess of those usually applied in clinical research. AtherosclerosisAnimal models of atherosclerosis have documented that all the constituents of the plaque produce and use ROS. Lesion formation is associated with the accumulation of lipid peroxidation products 1,2 and induction of inflammatory genes, 3 inactivation of NO · resulting in endothelial dysfunction, 4,5 activation of matrix metalloproteinases, 6 and increased smooth muscle cell growth. 7 Atherogenesis in rodents is accompanied by increasing lipid peroxidation in vivo. Thus, levels of the F 2 isoprostane (iP), iPF 2␣ -IV, are increased in both urine and aortic tissue as atherosclerosis evolves in both apolipoprotein E (ApoE)-and low-density lipoprotein (LDL) receptor-knockout mice. 8,9 Evidence exists for and against the efficacy of vitamin E in limiting atherogenesis. 10 -12 However, a rational basis for selection of the interventional regimens, or indeed the possibility of comparing treatment regimens across models and species by anything other than weight-corrected dosing, does not exist, pointing to the need for a much more rigorous approach to the development, application, and testing of antioxidant therapies. If a dosing regimen of vitamin E is selected on the basis of its ability to suppress elevated urinary iPF 2␣ -VI in atherosclerotic ApoE mice, vitamin E will retard atherosclerosis by Ϸ50% while leaving hypercholesterolemia unaffected. 8 However, administration of much lower doses of vitamin E to the same model failed to detect an impact on atherogenesis. 10 It is notew...

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Section: Ros and Vascular Disease: Human Studiesmentioning

confidence: 99%

Oxidative Stress and Cardiovascular Injury

2003

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“…A number of previous studies have shown that both cigarette smoking and smoke extract impair the nitric oxide synthase (NOS)-dependent reactivity of peripheral blood vessels (Mays et al, 1999;Ota et al, 1997;McVeigh et al, 1996;Celermajer et al, 1993). In addition, Fang et al (2003) noted that intravenous nicotine infusion impaired NOS-dependent dilatation in cerebral arterioles via the production of oxygen radicals, and suggesting that such changes might contribute to the pathogenesis of cerebrovascular abnormalities, including ischemic stroke.…”

Section: Introductionmentioning

confidence: 97%

Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats

Iida

Takenaka

et al. 2006

Life Sciences

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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: 92%

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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Ascorbic Acid Prevents Cigarette Smoke Injury to Endothelium-Dependent Arterial Relaxation

Cited by 32 publications

References 28 publications

Oxidative Stress and Cardiovascular Injury

Oxidative Stress and Cardiovascular Injury

Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats

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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