Impairment of Acetylcholine Relaxations by Malondialdehyde, a Marker of Lipid Peroxidation

Rodríguez-Martínez, María; Martı́nez-Orgado, José; Salaíces, Mercedes; Marín, Juan Eliseo Montoya

doi:10.1159/000159185

Cited by 13 publications

(9 citation statements)

References 32 publications

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“…However, no differences in basal free 3-nitrotyrosine levels were found between non-tolerant SHR and WKY. Nevertheless, a difference in ONOO À release between SHR and WKY cannot be excluded, since the protein-bound 3-nitrotyrosine concentration was not assessed in the present study and an increase in protein-bound 3-nitrotyrosine in aortas from aortic banding-induced hypertensive rats was recently demonstrated [34]. Neither treatment with NAC nor melatonin changed the free 3-nitrotyrosine level in nontolerant rats of both strains, but they prevented the rise of free 3-nitrotyrosine in coronary ef¯uent of tolerant SHR.…”

Section: Discussionmentioning

confidence: 84%

Effect of antioxidant treatments on nitrate tolerance development in normotensive and hypertensive rats

Cabassi¹,

Bouchard

Dumont

et al. 2000

Journal of Hypertension

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aObjectives To investigate the effect of chronic antioxidant treatments on the development of nitrate tolerance in spontaneously hypertensive (SHR) and normotensive Wistar±Kyoto (WKY) rats by evaluating (i) coronary vascular reactivity, (ii) lipid peroxidation (malondialdehyde), and (iii) peroxynitrite formation (3-nitrotyrosine).Methods Tolerance was induced in 16-week-old male SHR and WKY, by 4 days of continuous treatment with nitroglycerin patches. Two groups were orally pre-treated (2-weeks) with antioxidants: N-acetyl-L-cysteine (NAC) or melatonin. Effects of serotonin (5-HT) and sodium nitroprusside (SNP) perfusion were tested in isolated Langendorff-perfused hearts. 3-nitrotyrosine levels were measured in coronary sinus ef¯uent and malondialdehyde in plasma.Results Nitrate tolerance reduced SNP-induced dilation in both strains. This alteration was differently improved by antioxidants: melatonin was effective in SHR, whereas NAC was effective in WKY. Tolerance also reduced 5-HTmediated vasodilation in WKY, which was reversed by both antioxidants. By contrast, nitrate tolerance enhanced the vasoconstriction to 5-HT in SHR and both antioxidants prevented this response. Furthermore, tolerance was associated with higher malondialdehyde levels in both strains and with higher 3-nitrotyrosine levels in SHR. These changes were reversed by both antioxidants.Conclusions A participation of oxidative stress was suggested during nitrate tolerance development, since antioxidants prevented the increase in lipid peroxidation and improved vascular responses to SNP and 5HT. Differential effects of antioxidants on SNP-induced vasodilation in SHR and WKY may suggest distinct mechanisms of tolerance development in hearts from hypertensive and normotensive rats. An increased peroxynitrite generation, expressed by higher 3-nitrotyrosine levels, could contribute to nitrate tolerance in the coronary circulation of SHR.

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Section: Discussionmentioning

confidence: 84%

Effect of antioxidant treatments on nitrate tolerance development in normotensive and hypertensive rats

Cabassi¹,

Bouchard

Dumont

et al. 2000

Journal of Hypertension

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“…It has been demonstrated that MDA inhibits the endothelium-dependent vasorelaxation to acetylcholine in the tail artery of normal rats [32]. Additionally, NO also plays a major key role in the development of hyperdynamic circulation and portal hypertension in cirrhosis [18].…”

Section: Discussionmentioning

confidence: 99%

Increased Plasma Malondialdehyde in Patients with Viral Cirrhosis and Its Relationships to Plasma Nitric Oxide, Endotoxin, and Portal Pressure

et al. 2009

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“…Recently, we demonstrated, for the first time, that MDA produces a reduction of endothelium‐dependent relaxations to ACh in the tail artery from adult SD rats (6 months) (Rodríguez‐Martínez et al , 1996). In the present study, we have assessed the effect of age on the vascular actions of MDA, associated with age‐related changes in the blood prooxidant‐antioxidant state of the animals.…”

Section: Discussionmentioning

confidence: 96%

Role of lipid peroxidation and the glutathione‐dependent antioxidant system in the impairment of endothelium‐dependent relaxations with age

Rodríguez-Martínez¹,

Alonso²,

Redondo³

et al. 1998

British J Pharmacology

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1 Age-related changes in the blood prooxidant-antioxidant state, as well as its in¯uence on the relaxant responses to acetylcholine (ACh) were studied in the tail artery from 6-, 24-and 30-month-old SpragueDawley (SD) rats. 2 Malondialdehyde (MDA) plasma levels increased 2 and 3 times in 24-and 30-month-old rats, respectively, when compared with 6-month-old rats (0.43+0.09 mM). This increase was accompanied by an induction of 6-phosphogluconate dehydrogenase (6PG-DH) and glutathione reductase (GR) activities in red blood cells from 24-month-old rats. In 30-month-old rats, a further induction of these enzymatic activities, as well as glucose-6-phosphate dehydrogenase (G6P-DH) and glutathione peroxidase (GPx) activities was observed.3 No dierences with age were found in the concentration-response curves to ACh in isolated tail artery segments from 6-and 24-month-old rats precontracted with 0.3 mM noradrenaline (NA). However, a decrease in sensitivity to ACh-induced relaxation was observed in 30-month-old rats; EC 30 values were 3.5 (1.3 ± 8.0)610 77 M and 18.1 (8.9 ± 30.1)610 77 M for 6-and 30-month-old rats, respectively. Moreover, a decrease in maximum ACh relaxation (10 mM) was found in 30-month-old rats in comparison with that obtained in 6-month-old rats (58.5+3.9% and 42.5+3.4% of previous NA contraction, respectively). 4 Incubation of tail artery segments with MDA (0.5, 1 or 10 mM) caused a reduction of ACh-induced relaxations that was dierent in the three ages. Thus, the reduction of ACh-induced relaxations became signi®cant with 0.5 mM MDA in 6-, with 1 mM MDA in 24-, and with 10 mM MDA in 30-month-old rats. In addition, MDA did not cause a shift in the concentration-response curve to ACh, but a decrease in the maximum response. 5 Superoxide dismutase (SOD; 150 u ml 71 , a superoxide anion scavenger) reversed the inhibitory eect of MDA on ACh-induced relaxations at all ages studied. 6 We conclude that: (1) ageing produces an increase in lipid peroxidation process, as indicated by the increase in MDA plasma levels, that is accompanied by an induction of lipid peroxide detoxi®cation enzymes; (2) the changes in prooxidant-antioxidant equilibrium with age contribute, at least partially, to the impairment of the relaxant responses evoked by ACh; and (3) the eect of MDA appears to be mediated by superoxide anion at all ages studied.

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Impairment of Acetylcholine Relaxations by Malondialdehyde, a Marker of Lipid Peroxidation

Cited by 13 publications

References 32 publications

Effect of antioxidant treatments on nitrate tolerance development in normotensive and hypertensive rats

Effect of antioxidant treatments on nitrate tolerance development in normotensive and hypertensive rats

Increased Plasma Malondialdehyde in Patients with Viral Cirrhosis and Its Relationships to Plasma Nitric Oxide, Endotoxin, and Portal Pressure

Role of lipid peroxidation and the glutathione‐dependent antioxidant system in the impairment of endothelium‐dependent relaxations with age

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