Low-dose chronic lead exposure increases systolic arterial pressure and vascular reactivity of rat aortas

Silveira, Edna Aparecida; Siman, Fabiana Dayse Magalhães; Faria, Thaís de Oliveira; Vescovi, Marcos Vinícius A.; Furieri, Lorena Barros; Lizardo, Juliana Hott de Fúcio; Stefanon, Ivanita; Padilha, Alessandra Simão; Vassallo, Dalton Valentim

doi:10.1016/j.freeradbiomed.2013.11.021

Cited by 55 publications

(47 citation statements)

References 47 publications

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“…Furthermore, BP also increased, which confirms our previous reports that low to moderate levels of lead intoxication are related to a slight elevation of BP in rats [7,24] and population studies showing a relationship between blood lead levels and hypertension [27,28].…”

Section: Discussionsupporting

confidence: 89%

“…We recently demonstrated that chronic lead acetate administration in rats, leading to blood concentrations as low as 10-20 lg/dL, elevates BP and increases vascular reactivity [7][8][9]. These results reinforce the idea of hazardous lead effects even at low levels.…”

Section: Introductionsupporting

confidence: 57%

“…Additionally, it is already known that the lower sensitivity of the baroreflex promoted by angiotensin II plays an important role in the pathophysiology of hypertension, mainly by central actions, characterised by vasopressin release, sympathetic activation and baroreflex inhibition [46,47]. In this regard, previous studies by our research group and others [7,13,48] showed evidence that peripheral reninangiotensin system activity is increased by lead.…”

Section: Cardiovasc Toxicolmentioning

confidence: 62%

“…The rat blood volume was calculated according to Lee and Blaufox [23]. This exposure protocol was proven to increase BP in rats [7,24]. Lead acetate, Pb(CH 3 COO) 2 , was purchased from Sigma Chemical Co., USA.…”

Section: Animal Model Of Chronic Lead Exposurementioning

confidence: 99%

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Low-level Chronic Lead Exposure Impairs Neural Control of Blood Pressure and Heart Rate in Rats

et al. 2016

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Lead (Pb) induces adverse effects when it chronically accumulates in the body, including effects on the nervous and cardiovascular systems. Wistar rats were exposed to lead acetate for 30 days (first dose 4 µg/100 g followed by 0.05 µg/100 g/day, i.m.) to investigate the cardiovascular system impact on the autonomic control. The femoral artery and vein were catheterised to perform hemodynamic evaluations in awake rats: heart rate variability (HRV), baroreflex sensitivity, cardiopulmonary reflex and hemodynamic responses to vagal and sympathetic pharmacological blockade. Rats exposed to Pb exhibited a higher blood pressure and reduced HRV in the time domain when compared to the saline-injected group. Spectral analysis of the HRV in the frequency-domain showed an augmented low-frequency component of the spectrum. Methylatropine and atenolol administration suggest increased sympathetic tone and reduced vagal tone on the control of heart rate. Chronic Pb exposure decreased the sensitivity of the baroreflex without significantly changing the cardiopulmonary reflex. This study demonstrated for the first time in an animal model of a controlled, low-dose chronic lead exposure that cardiovascular changes, such as arterial hypertension, are accompanied by impaired autonomic control of the cardiovascular system, as characterised by reduced baroreflex sensitivity and a sympathovagal imbalance.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionsupporting

confidence: 57%

Section: Cardiovasc Toxicolmentioning

confidence: 62%

Section: Animal Model Of Chronic Lead Exposurementioning

confidence: 99%

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Low-level Chronic Lead Exposure Impairs Neural Control of Blood Pressure and Heart Rate in Rats

et al. 2016

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“…Nevertheless, there are still a number of issues with the previous usage of Pb resulting in a legacy of widespread contamination [29]. Present day Pb blood levels are still between 50 to 200 times greater than the blood Pb concentrations of preindustrial humans at about 0.8 nM (0.016 μg/dL) [30][31][32]. Advances in toxicology have highlighted the increasingly smaller concentrations that Pb is known to cause adverse effects [33,34].…”

Section: Introductionmentioning

confidence: 99%

The voltammetric behaviour of lead at a hand drawn pencil electrode and its trace determination in water by stripping voltammetry

Honeychurch

2015

Anal. Methods

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Advanced oxidation protein products induce hepatocyte epithelial–mesenchymal transition via a ROS‐dependent, TGF‐β/Smad signaling pathway

Sun

Xie

Zhang

et al. 2017

Cell Biology International

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Epithelial-mesenchymal transition (EMT) occurs during the progression of liver fibrosis in response to chronic liver injury. However, the molecular mechanism underlying the regulation of hepatocyte EMT remains unclear. The aim of this study was to determine whether advanced oxidation protein products (AOPP) had an effect on hepatocyte EMT. The human L02 hepatocyte cell line and hepatocytes from normal Sprague-Dawley rats were challenged with AOPP treatment in both in vitro and in vivo studies. The expression of cell and molecular markers of EMT in L02 hepatocytes were studied using Western blotting, and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assays. Hepatocyte migratory potential was analyzed using a wound healing assay. Intracellular reactive oxygen species (ROS) were detected using the dichlorofluorescein (DCF) assay. In liver tissue sections, expression of EMT markers was evaluated using immunohistochemistry, and collagen was assessed using histochemical staining with Masson's trichrome. The findings were that AOPP treatment resulted in EMT in hepatocytes, which was associated with reduced expression of E-cadherin, increased expression of vimentin, increased deposition of collagen protein, and enhanced cell migration in vivo and in vitro. AOPP was also found to promote migration in L02 cells, and to promote the production of ROS and the activation of TGF-βR and Smad signaling. Inhibition of the generation of intracellular ROS and TGF-β receptor blocking could reverse AOPP-induced EMT in hepatocytes. This study has identified a novel mechanism in the regulation of hepatocyte EMT, and the findings may have implications for the control of liver fibrosis.

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Low-dose chronic lead exposure increases systolic arterial pressure and vascular reactivity of rat aortas

Cited by 55 publications

References 47 publications

Low-level Chronic Lead Exposure Impairs Neural Control of Blood Pressure and Heart Rate in Rats

Low-level Chronic Lead Exposure Impairs Neural Control of Blood Pressure and Heart Rate in Rats

The voltammetric behaviour of lead at a hand drawn pencil electrode and its trace determination in water by stripping voltammetry

Advanced oxidation protein products induce hepatocyte epithelial–mesenchymal transition via a ROS‐dependent, TGF‐β/Smad signaling pathway

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