Lead-induced hypertension: Role of oxidative stress

Vaziri, Nosratola D.; Sica, Domenic A.

doi:10.1007/s11906-004-0027-3

Cited by 108 publications

(98 citation statements)

References 82 publications

(92 reference statements)

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“…There is very strong evidence that lead decreases the functional availability of the potent vasodilator NO, most likely through direct or indirect mechanisms involving oxidative stress [34]. In the current study, the plasma levels of NO were significantly lower in hypertensive patients than controls.…”

Section: Discussioncontrasting

confidence: 41%

“…Lead may cause enhanced sympathetic nerve activity with increases in circulating epinephrine and norepinephrine levels in conjunction with decreased density of vasodilating beta 2 adrenergic receptors [33]. Chronic low-level exposure to lead results in increased activity of angiotensin converting enzyme activity and increases in plasma renin, angiotensin II, and aldosterone levels [34]. Plasma kininase I and II levels are higher during Pb exposure.This can lead to decreases in plasma bradykinin levels resulting in a reduction in endothelial NO production [35].…”

Section: Discussionmentioning

confidence: 99%

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Relationship Between Blood Lead Level and Elevated Blood Pressure in Hypertensive Patients: Implication of Nitric Oxide

Meki¹

2011

TONOJ

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Abstract:The correlation between the blood lead (B-Pb ) levels and the values of blood pressure in hypertensive patients was investigated. Moreover, plasma levels of nitric oxide (NO), total antioxidants (TAOX) and malondialdehyde (MDA) were detected to investigate the correlations between the measured parameters and B-Pb levels in hypertensive patients. Fifty-five hypertensive patients were compared with fifty-three age and sex matched control group. The B-Pb levels were detected by flame atomic absorption spectrometry. The plasma levels of NO, TAOX and MDA were measured by colorimetric methods. In the hypertensive patients, B-Pb levels were significantly higher than controls. Concomitantly, the plasma levels of MDA were significantly increased while the plasma levels of NO and TAOX were significantly reduced in the hypertensive patients in comparison with controls. There were significant positive correlations between B-Pb and each of MDA, systolic and diastolic blood pressure. Conversely, a significant negative correlation was found between BPb and NO. Our study indicated that B-Pb level was associated with elevated blood pressure as well as oxidative stress in hypertensive patients. Moreover, the negative correlation between the B-Pb level and NO level may clarify their implication in cardiovascular disease and hypertension.

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Section: Discussioncontrasting

confidence: 41%

Section: Discussionmentioning

confidence: 99%

Relationship Between Blood Lead Level and Elevated Blood Pressure in Hypertensive Patients: Implication of Nitric Oxide

Meki¹

2011

TONOJ

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“…Oxidative stress develops when the well-regulated balance between prooxidants and antioxidants becomes uncontrolled and tips in favor of pro-oxidants. Oxidative stress is a major contributor to the aging process (26) and appears to be a common feature of hypertensive disorders from diverse origins (9,(27)(28)(29). ROS have also been shown to be involved in cardiac hypertrophy induced by several stimuli, such as mechanical stretch, endothelin and angiotensin II (30).…”

Section: Discussionmentioning

confidence: 99%

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

et al. 2008

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The aim of this work was to assess the possible correlation between oxidative damage and the development of cardiac hypertrophy in heart tissue from young (40-d-old) and older (4-, 11-and 19-month-old) spontaneously hypertensive rats (SHR) in comparison with age-matched Wistar (W) rats. To this end, levels of thiobarbituric acid reactive substances (TBARS), nitrotyrosine contents, NAD(P)H oxidase activity, superoxide production, and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were determined. Compared to age-matched normotensive rats, SHR showed a significant increase in systolic blood pressure from 40 d of age and left ventricular hypertrophy (LVH) was significantly evident from 4 months of age. W rats (11-and 19-month-old) also showed an increase in LVH with aging. TBARS and nitrotyrosine levels were similar in young rats from both strains and were significantly increased with age in both strains, with the values in SHR being significantly higher than those in age-matched W rats. NAD(P)H activity was similar in young SHR and W rats, whereas it was higher in aged SHR compared with age-matched W rats. Compared to W rats, superoxide production was higher in aged SHR, and was abolished by NAD(P)H inhibition with apocynin. CAT activity was increased in the hearts of 4-month-old SHR compared to age-matched W rats and was decreased in the hearts of the oldest SHR compared to the oldest W rats. SOD and GPx activities decreased in both rat strains with aging. Moreover, an increase in collagen deposition with aging was evident in both rat strains. Taken together, these data showed that aged SHR exhibited higher cardiac hypertrophy and oxidative damage compared to W rats, indicating that the two undesirable effects are associated. That is, oxidative stress appears to be a cause and/or consequence of hypertrophy development in this animal model. (Hypertens Res 2008; 31: 1465-1476)

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“…In the neural tissue, lead acts by inhibiting Na,K-ATPase, increasing the production of free radicals, which results in neural lesions (4,25). A hypertensive effect was also reported and the action of lead is related to impairment of endothelial function and also to the production of free radicals (4,13,26). An increased production of angiotensin II has also been reported as a mechanism to induce hypertension (15).…”

Section: Discussionmentioning

confidence: 99%

Lead reduces tension development and the myosin ATPase activity of the rat right ventricular myocardium

Vassallo

Lebarch

Moreira

et al. 2008

Braz J Med Biol Res

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Lead (Pb 2+ ) poisoning causes hypertension, but little is known regarding its acute effects on cardiac contractility. To evaluate these effects, force was measured in right ventricular strips that were contracting isometrically in 45 male Wistar rats (250-300 g) before and after the addition of increasing concentrations of lead acetate (3,7,10,30, 70, 100, and 300 µM) to the bath. Changes in rate of stimulation (0.1-1.5 Hz), relative potentiation after pauses of 15, 30, and 60 s, effect of Ca 2+ concentration (0.62, 1.25, and 2.5 mM), and the effect of isoproterenol (20 ng/mL) were determined before and after the addition of 100 µM Pb 2+ . Effects on contractile proteins were evaluated after caffeine treatment using tetanic stimulation (10 Hz) and measuring the activity of the myosin ATPase. Pb 2+ produced concentration-dependent force reduction, significant at concentrations greater than 30 µM. The force developed in response to increasing rates of stimulation became smaller at 0.5 and 0.8 Hz. Relative potentiation increased after 100 µM Pb 2+ treatment. Extracellular Ca 2+ increment and isoproterenol administration increased force development but after 100 µM Pb 2+ treatment the force was significantly reduced suggesting an effect of the metal on the sarcolemmal Ca 2+ influx. Concentration of 100 µM Pb 2+ also reduced the peak and plateau force of tetanic contractions and reduced the activity of the myosin ATPase. Results showed that acute Pb 2+ administration, although not affecting the sarcoplasmic reticulum activity, produces a concentration-dependent negative inotropic effect and reduces myosin ATPase activity. Results suggest that acute lead administration reduced myocardial contractility by reducing sarcolemmal calcium influx and the myosin ATPase activity. These results also suggest that lead exposure is hazardous and has toxicological consequences affecting cardiac muscle.

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Lead-induced hypertension: Role of oxidative stress

Cited by 108 publications

References 82 publications

Relationship Between Blood Lead Level and Elevated Blood Pressure in Hypertensive Patients: Implication of Nitric Oxide

Relationship Between Blood Lead Level and Elevated Blood Pressure in Hypertensive Patients: Implication of Nitric Oxide

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Lead reduces tension development and the myosin ATPase activity of the rat right ventricular myocardium

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