Vitamin C increases the prostacyclin production and decreases the vascular lesions in experimental atherosclerosis in rabbits

Beetens, Johan; Coene, M.‐C.; Verheyen, A.; Zonnekeyn, L; Herman, Arnold G.

doi:10.1016/0090-6980(86)90003-1

Cited by 30 publications

(5 citation statements)

References 25 publications

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“…While the means by which ascorbate prevents tolerance remain to be determined, others have suggested that Vit-C could ( a ) directly affect superoxide production by the NADPH oxidoreductase; ( b ) scavenge superoxide directly, and thereby decrease nitric oxide inactivation; ( c ) increase ni- trosothiol formation by protecting plasma thiols from oxidation; and ( d ) suppress peroxynitrite-mediated inactivation of target enzymes (4,7,(13)(14)(15)(16)(17)(27)(28)(29). Other factors, including possible effects on GTN biotransformation, the neurohumoral axis, prostacyclin generation, leukocyte aggregation, oxidized LDL generation, or platelet-activating factor mimetics, cannot be ruled out (30)(31)(32)(33)(34)(35)(36).…”

Section: Discussionmentioning

confidence: 99%

Dietary supplement with vitamin C prevents nitrate tolerance.

Bassenge¹,

Fink²,

Skatchkov³

et al. 1998

J. Clin. Invest.

129

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Enhanced formation of superoxide radicals has been proposed to play a major role in the development of nitrate tolerance in humans. We tested the effects of vitamin C (Vit-C) supplementation on glyceroltrinitrate (GTN)-induced hemodynamic effects during 3-d nonintermittent transdermal administration of GTN (0.4 mg/h) in nine healthy subjects. Tolerance development was monitored by changes in arterial pressure, dicrotic digital pulse pressure, and heart rate. Studies with GTN, Vit-C, or GTN/Vit-C were successively carried out at random in three different series in the same subjects. GTN treatment caused an immediate rise in arterial conductivity (a/b ratio of dicrotic pulse), but within 2 d of initiating GTN, the a/b ratio progressively decreased and reached basal levels. In addition, there was a progressive loss of the orthostatic decrease in blood pressure. However, coadministration of Vit-C and GTN fully maintained the GTN-induced changes in the orthostatic blood pressure, and the rise of a/b ratio was augmented by 310% for the duration of the test period. Changes in vascular tolerance in GTN-treated subjects were paralleled by upregulation of the activity of isolated platelets, which was also reversed by

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Section: Discussionmentioning

confidence: 99%

Dietary supplement with vitamin C prevents nitrate tolerance.

Bassenge¹,

Fink²,

Skatchkov³

et al. 1998

J. Clin. Invest.

129

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“…This view is strengthened by the observation that the receptor-induced release of other endothelial products, such as prostacyclin, is attenuated as well. 104,105 In this respect, it has been demonstrated that the pertussis toxin-sensitive G i protein signalling pathway, which is employed by serotonin to elicit endothelium-dependent relaxation in the pig coronary artery, is impaired in the early stages of the atherosclerotic process. 106 Several studies have demonstrated that incubation of vessel segments with lipoproteins, and in particular with oxLDL, inhibited endothelium-dependent relaxation in a way similar to hypercholesterolaemia in vivo (reviewed by Flavahan 99 ).…”

Section: Explanations For the Defective No Signalling Pathwaymentioning

confidence: 99%

Nitric oxide function in atherosclerosis

Matthys

Bult

1997

Mediators of Inflammation

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Atherosclerosis is a chronic inflammatory process in the intima of conduit arteries, which disturbs the endothelium-dependent regulation of the vascular tone by the labile liposoluble radical nitric oxide (NO) formed by the constitutive endothelial nitric oxide synthase (eNOS). This defect predisposes to coronary vasospasm and cardiac ischaemia, with anginal pain as the typical clinical manifestation. It is now appreciated that endothelial dysfunction is an early event in atherogenesis and that it may also involve the microcirculation, in which atherosclerotic lesions do not develop. On the other hand, the inflammatory environment in atherosclerotic plaques may result in the expression of the inducible NO synthase (iNOS) isozyme. Whether the dysfunction in endothelial NO production is causal to, or the result of, atherosclerotic lesion formation is still highly debated. Most evidence supports the hypothesis that constitutive endothelial NO release protects against atherogenesis e.g. by preventing smooth muscle cell proliferation and leukocyte adhesion. Nitric oxide generated by the inducible isozyme may be beneficial by replacing the failing endothelial production but excessive release may damage the vascular wall cells, especially in combination with reactive oxygen intermediates.

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“…Thus zinc deficiency in rats is reported to reduce the response to prostacyclin (Browning et al, 1987). Vitamin C is reported to stimulate prostacyclin production in both animal and human cells (Beetens et al, 1986;Toivanen, 1987). The available information about the effect of these other nutrients on hypertension is at present fragmentary and is in no way comparable to the published data from many countries about magnesium and thiamin.…”

Section: Are Other Mineral and Vitamin Deficiencies Associated With Pmentioning

confidence: 99%

Magnesium and Other Nutrient Deficiencies as Possible Causes of Hypertension and Low Birthweight

Wynn¹,

Wynn²

1988

Nutr Health

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7.2 per cent of babies born in England and Wales in 1986 had birthweights below 2,500 g. Low birthweight and hypertension are associated. European trials have reported that oral supplementation with physiological amounts of magnesium during pregnancy reduces pregnancy hypertension and also miscarriage, preterm birth and fetal growth retardation. Magnesium deficiency causes hypertension and low birthweight in animals. In humans deficiency of thiamin and other B vitamins has also been reported to cause pregnancy hypertension and low birthweight. Magnesium and B vitamins are essential for the same biochemical reactions in energy metabolism. There is evidence that magnesium consumption of substantial numbers of women in Europe and North America is too low to support a healthy pregnancy. Magnesium and thiamin are lost in processing many foods. British trials of magnesium supplementation are advocated. It is suggested that more attention should be given to magnesium in nutritional advice.

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Vitamin C increases the prostacyclin production and decreases the vascular lesions in experimental atherosclerosis in rabbits

Cited by 30 publications

References 25 publications

Dietary supplement with vitamin C prevents nitrate tolerance.

Dietary supplement with vitamin C prevents nitrate tolerance.

Nitric oxide function in atherosclerosis

Magnesium and Other Nutrient Deficiencies as Possible Causes of Hypertension and Low Birthweight

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