Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers

Kugiyama, Kiyotaka; Yasue, Hirofumi; Ohgushi, Masamichi; Motoyama, Takeshi; Kawano, Hiroaki; Inobe, Yoshito; Hirashima, Osamu; Sugiyama, Seigo

doi:10.1016/s0735-1097(96)00325-7

Cited by 129 publications

(74 citation statements)

References 41 publications

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“…Exposure to media conditioned by the combustion of cigarette papers alone had no effect on 3 H-L-arginine uptake (99Ϯ12%). In contrast to the actions of CSE, exposure of ECs to 100 mmol/L H 2 O 2 was entirely without effect on 3 …”

Section: Effects Of Cse On Intracellular Arginine Related Metabolitementioning

confidence: 71%

“…In these studies, there was a 38% reduction in the accumulation of 3 H-L-arginine ( Figure 1b). In conjunction, as determined by RT-PCR analysis, there was a 34% reduction in CAT1 mRNA expression (PϽ0.01; Figure 1c).…”

Section: H-l-arginine Uptake (Data Not Shown)mentioning

confidence: 75%

“…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.…”

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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: Effects Of Cse On Intracellular Arginine Related Metabolitementioning

confidence: 71%

Section: H-l-arginine Uptake (Data Not Shown)mentioning

confidence: 75%

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confidence: 99%

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Adverse Effects of Cigarette Smoke on NO Bioavailability

et al. 2006

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“…All of the study subjects had angiographically normal coronary arteries (Ͻ10% stenosis) and no coronary spasm during intracoronary infusion of acetylcholine (ACh). 8,9 All medications were withdrawn Ն3 days before study. None of the study subjects had taken pharmacological doses of antioxidants for at least 1 month before the study.…”

Section: Study Subjectsmentioning

confidence: 99%

“…8,9 In brief, the trunk of the left anterior descending coronary artery (LAD) was divided into proximal and distal segments of equal length. The luminal diameter at the center of each segment was measured quantitatively with the use of a computer-assisted coronary angiographic analysis system (Cardio 500, Kontron Instruments) by 2 observers blinded to the study protocol.…”

Section: Quantitative Coronary Angiography and Measurement Of Coronarmentioning

confidence: 99%

Intracoronary Infusion of Reduced Glutathione Improves Endothelial Vasomotor Response to Acetylcholine in Human Coronary Circulation

et al. 1998

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Background-Oxygen free radicals have been shown to cause endothelial vasomotor dysfunction. This study examined the effect of reduced glutathione (GSH), an antioxidant, on human coronary circulation. Methods and Results-Responses of epicardial diameter and blood flow of the left anterior descending coronary artery to intracoronary infusion of acetylcholine (ACh, 50 g/min) were measured by quantitative coronary angiography and Doppler flow-wire technique, respectively, before and during combined intracoronary infusion of GSH (50 mg/min) or saline in 26 subjects with no significant coronary stenosis. GSH infusion suppressed the constrictor response of epicardial diameter to ACh and enhanced the increase in blood flow response to ACh. Furthermore, GSH potentiated the coronary dilator effect of nitroglycerin. A beneficial effect of GSH on the epicardial diameter response to ACh was observed in a subgroup of subjects with Ն1 coronary risk factors but not in a subgroup without risk factors. Saline infusion did not have any effects. Conclusions-The results indicate that GSH improved coronary endothelial vasomotor function, particularly in subjects with coronary risk factors, and it potentiated the vasodilator effect of nitroglycerin in human coronary arteries.

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Endotheliale Dysfunktion als Ursache der kardialen Vaskulopathie

Lauer¹,

Kelm²

Diabetes Und Herz

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Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers

Cited by 129 publications

References 41 publications

Adverse Effects of Cigarette Smoke on NO Bioavailability

Adverse Effects of Cigarette Smoke on NO Bioavailability

Intracoronary Infusion of Reduced Glutathione Improves Endothelial Vasomotor Response to Acetylcholine in Human Coronary Circulation

Endotheliale Dysfunktion als Ursache der kardialen Vaskulopathie

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