Magnesium Modulates Contractile Responses of Rat Aorta to Thiocyanate: A Possible Relationship to Smoking-Induced Atherosclerosis

Li, Wenyan; Zheng, Tao; Altura, Bella T.; Altura, Burton M.

doi:10.1006/taap.1999.8666

Cited by 7 publications

(5 citation statements)

References 49 publications

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“…Thus, in smoker rats the effect of increased endothelin release at rest coupled with a reduced basal production of NO would lead to increased vascular tone. Other effects of reactive oxygen species such as altering Ca2 + extrusion (Liu et al, 2002;, increasing intracellular calcium ([Ca 2+ ]i) (Li et al, 1999) and reducing K + channel activity (Iida et al, 1998) can also increase vascular reactivity.…”

Section: Vasoconstriction Studymentioning

confidence: 99%

Increased vascular contractility in isolated vessels from cigarette smoking rats is mediated by basal endothelin release

Rahman

Elmi

Chang

et al. 2007

Vascular Pharmacology

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The effect of chronic cigarette smoking on endothelin modulation of vascular contraction, and CYP enzyme levels was studied in 20 male Sprague-Dawley rats. The animals were divided equally into smoking and non-smoking groups. The smoking group was exposed to 6 research cigarettes per rat per day 5 days a week for 16 weeks. The control group was sham smoked. Functional contractile studies were performed in aortas and carotid arteries to determine the regulation of vascular tone by basal release of endothelin. Liver samples were analyzed for CYP1A1 and CYP1A2 gene expression by RT-PCR. Plasma samples were assessed for endothelin-1 (ET-1) level by enzyme immuno assay (EIA). Treatment of aortas and carotid arteries with bosentan, the dual endothelin receptor antagonist, caused a significant reduction in constrictor responses of smoking rats, indicating, increase greater regulation of tone by endothelin in smoker rats compared to controls. There was a greater expression of the cytochrome P450-liver enzymes (CYP1A1 and CYP1A2) in smoker rats. Body weight gain was also significantly decreased in smoker rats. We conclude that increased endothelin release in smoker rats significantly contributes to increased arterial tone and so contribute to the cardiovascular pathophysiology associated with cigarette smoking, such as increased vascular muscularization, increased contraction, decreased dilation and possibly vasospasm.

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Section: Vasoconstriction Studymentioning

confidence: 99%

Increased vascular contractility in isolated vessels from cigarette smoking rats is mediated by basal endothelin release

Rahman

Elmi

Chang

et al. 2007

Vascular Pharmacology

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“…The described SCN − -induced contraction of vascular smooth muscle was also observed in rat portal veins (Zhang et al, 1991). However, incubation in the absence of extracellular Ca2+ abolished the SCN − -induced contractile responses (Standley et al, 1996, Li et al, 1999). Engström and Sehlin (1996) observed similar vasoconstrictory effects of SCN − in their rat tail artery perfusion model.…”

Section: Discussionmentioning

confidence: 97%

“…There is also evidence that atherosclerotic disease progression in the aorta is much more rapid when serum SCN − levels are increased (Scanlon et al, 1996, Botti et al, 1996). Because of the link between elevated serum SCN − concentrations and atherosclerotic disease, the effect of SCN − has been of particular interest (Li et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Melatonin attenuates thiocyanate-induced vasoconstriction in aortic rings

Prusa

Plass

2017

Saudi Pharmaceutical Journal

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Cigarette smoking not only has a carcinogenic effect but also leads to an increase in arterial blood pressure. Besides its main components, i.e. nicotine, tar, and carbon monoxide, cigarette smoke also contains thiocyanate. Thiocyanate anions (SCN) arise from the detoxification of hydrogen cyanide and its plasma concentrations were found to correlate significantly with cigarette consumption. There is also evidence that atherosclerotic disease progression is much more rapid when serum SCN levels are increased. Melatonin, a non-toxic indolamine with various physiologic functions, is believed to protect against inflammatory processes and oxidative stress. It has been demonstrated that melatonin serves as free radical scavenger and represents a potent antioxidant. Therefore, it is believed that melatonin with its atheroprotective effects may be useful either as a sole therapy or in conjunction with others. The aim of this study was to quantify the thiocyanate-induced vasomotor response in aortic tissue and further to examine the potential of melatonin in affecting the generated vasoreactivity. Aortic rings of adult male normotensive Wistar rats were cut into 4-mm rings. Following the administration of thiocyanate in various concentrations, vasomotor response of aortic vessel segments was measured. To assess the effect of melatonin on vasomotor activity, organ bath concentrations were modulated from 60 to 360 pM, which corresponds to physiologic plasma up to the levels of patients with regular oral intake of 3 mg of melatonin as a supplement. Thirty-six rat aortic rings were studied. When exposed to thiocyanate, vessel segments revealed vasoconstriction in a concentration-dependent manner. In rings which were preincubated with melatonin at a concentration of 360 pM, a 56.5% reduction of effect size could be achieved (4.09 ± 1.22 mN versus 9.41 ± 1.74 mN, P < 0.0001). Additionally, administration of 360 pM melatonin at a norepinephrine concentration of 80 mM resulted in a relaxation of 10.9 ± 2.2%. The vasodilatatory effect of melatonin was significantly reduced to 1.3 ± 0.5% when concentration of norepinephrine was doubled (P < 0.002). This study indicates that vessel segments that were exposed to thiocyanate responded with a dose-dependent vasoconstriction. The effect could be markedly attenuated in segments preincubated in melatonin.

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“…These findings are consistent with risks from Mg deficiency among smokers reported in several epidemiological studies [54][55][56] . Poor Mg status, together with long-term exposure to thiocyanate anions among smokers, accelerates the atherosclerotic processes in animal models 57 . Moreover, a randomized clinical trial found that Mg deficiency accelerates the development of nicotine addiction through increasing the Mg dependent N-Methyl-D-aspartic acid or N-Methyl-D-aspartate receptors activity 58 .…”

Section: Discussionmentioning

confidence: 99%

Serum magnesium concentrations and all-cause, cardiovascular, and cancer mortality among U.S. adults: Results from the NHANES I Epidemiologic Follow-up Study

et al. 2018

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Magnesium Modulates Contractile Responses of Rat Aorta to Thiocyanate: A Possible Relationship to Smoking-Induced Atherosclerosis

Cited by 7 publications

References 49 publications

Increased vascular contractility in isolated vessels from cigarette smoking rats is mediated by basal endothelin release

Increased vascular contractility in isolated vessels from cigarette smoking rats is mediated by basal endothelin release

Melatonin attenuates thiocyanate-induced vasoconstriction in aortic rings

Serum magnesium concentrations and all-cause, cardiovascular, and cancer mortality among U.S. adults: Results from the NHANES I Epidemiologic Follow-up Study

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