Low-Level Lead Exposure Increases Systolic Arterial Pressure and Endothelium-Derived Vasodilator Factors in Rat Aortas

Fiorim, Jonaína; Júnior, Rogério Faustino Ribeiro; Silveira, Edna Aparecida; Padilha, Alessandra Simão; Vescovi, Marcos Vinícius A.; Jesus, Honério Coutinho de; Stefanon, Ivanita; Salaíces, Mercedes; Vassallo, Dalton Valentim

doi:10.1371/journal.pone.0017117

Cited by 50 publications

(47 citation statements)

References 48 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%

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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%

“…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%

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

et al. 2016

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“…A similar increase of vascular reactivity was obtained with lead treatments for 30 days or more (57). However, exposure of rats to low lead concentrations for 7 days decreased the contractile response of aortic rings to phenylephrine (58). These findings confirm previous reports clearly suggesting that the effects of lead are concentration and time dependent (32).…”

Section: Effects Of Heavy Metals On Vascular Reactivity Changes In Vasupporting

confidence: 89%

“…A short-term exposure to low lead concentrations, however, reduces vascular reactivity and seems to stimulate K + channels in vascular smooth muscle cells (58). Again, the effects of gadolinium on EDHF activity have not been described.…”

Section: Effects Of Mercury Lead and Gadolinium On Endothelial Modulmentioning

confidence: 99%

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Toxic effects of mercury, lead and gadolinium on vascular reactivity

Vassallo

Simões

Furieri

et al. 2011

Braz J Med Biol Res

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Heavy metals have been used in a wide variety of human activities that have significantly increased both professional and environmental exposure. Unfortunately, disasters have highlighted the toxic effects of metals on different organs and systems. Over the last 50 years, the adverse effects of chronic lead, mercury and gadolinium exposure have been underscored. Mercury and lead induce hypertension in humans and animals, affecting endothelial function in addition to their other effects. Increased cardiovascular risk after exposure to metals has been reported, but the underlying mechanisms, mainly for short periods of time and at low concentrations, have not been well explored. The presence of other metals such as gadolinium has raised concerns about contrast-induced nephropathy and, interestingly, despite this negative action, gadolinium has not been defined as a toxic agent. The main actions of these metals, demonstrated in animal and human studies, are an increase of free radical production and oxidative stress and stimulation of angiotensin I-converting enzyme activity, among others. Increased vascular reactivity, highlighted in the present review, resulting from these actions might be an important mechanism underlying increased cardiovascular risk. Finally, the results described in this review suggest that mercury, lead and gadolinium, even at low doses or concentrations, affect vascular reactivity. Acting via the endothelium, by continuous exposure followed by their absorption, they can increase the production of free radicals and of angiotensin II, representing a hazard for cardiovascular function. In addition, the actual reference values, considered to pose no risk, need to be reducedResearch supported by CAPES and CNPq/FAPES/ FUNCITEC (#39767531/07), Brazil, and MCINN (#SAF 2009-07201) and ISCIII (Red RECAVA, #RD06/0014/0011), Spai

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Lead acetate may cause erectile dysfunction by modulating NO/cGMP pathway in rat corpus cavernosum

Senbel

Helmy

2013

Cell Biol Toxicol

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Despite the fact that metal toxicity has been widely reported in industrial toxicological studies, very little has been reported about the effect of lead exposure on erectile function. This study investigated the effect of lead on erectile function in rats and aimed to preliminarily test the mechanisms by which it might affect erection. Rats were injected with lead acetate (0.25-2 mg/kg) intraperitoneally for 21 days. Intracavernosal pressure/mean arterial pressure (ICP/MAP) next to nerve stimulation; nitrite/nitrate; malonaldehyde; and reduced glutathione levels and superoxide dismutase activity in the corpus cavernosum, kidney, and brain were measured in addition to creatinine, urea, and testosterone. For acute studies, rats were injected intravenously with lead acetate, and then ICP/MAP was recorded for 45 min. Subacute treatment significantly reduced erection with significant elevation of malonaldehyde and reduction of nitrite/nitrate levels in the corpus cavernosum. In acute studies, lead (2 and 5 mg/kg) reduced neurogenic erections by 28.42 ± 3.76 and 96.84 ± 8.52%, respectively, an effect that was masked in the presence of NG-nitro-L-arginine, tetraethyl ammonium, or methylene blue, but not zinc protoporphyrine, and reversed by vitamin C and partially by sildenafil. Lead acetate may inhibit the erectile process in rats. Besides its prooxidant effect and consequent inactivation of nitric oxide, lead may negatively modulate the action of nitric oxide on guanylate cyclase and potassium channels.

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Low-Level Lead Exposure Increases Systolic Arterial Pressure and Endothelium-Derived Vasodilator Factors in Rat Aortas

Cited by 50 publications

References 48 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

Toxic effects of mercury, lead and gadolinium on vascular reactivity

Lead acetate may cause erectile dysfunction by modulating NO/cGMP pathway in rat corpus cavernosum

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