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Environ Res. 2017 May;155:182-192. doi: 10.1016/j.envres.2017.02.022. Epub 2017 Mar 10.

The cessation of the long-term exposure to low doses of mercury ameliorates the increase in systolic blood pressure and vascular damage in rats.

Author information

1
Postgraduate Program in Biochemistry, Universidade Federal do Pampa, Uruguaiana, RS, Brazil.
2
Postgraduate Program in Biochemistry, Universidade Federal do Pampa, Uruguaiana, RS, Brazil; Department of Basic Health Sciences, Universidad Rey Juan Carlos, Alcorcón, Spain; Bioactivity and Food Analysis Laboratory, Instituto de Investigación en Ciencias de la Alimentación, Madrid, Spain; Department of Physiological Sciences, Universidade Federal do Espírito Santo, Vitória, ES, Brazil; Department of Pharmacology, Universidad Autónoma de Madrid, Madrid, Spain.
3
Department of Basic Health Sciences, Universidad Rey Juan Carlos, Alcorcón, Spain.
4
Bioactivity and Food Analysis Laboratory, Instituto de Investigación en Ciencias de la Alimentación, Madrid, Spain.
5
Department of Physiological Sciences, Universidade Federal do Espírito Santo, Vitória, ES, Brazil.
6
Department of Pharmacology, Universidad Autónoma de Madrid, Madrid, Spain.
7
Postgraduate Program in Biochemistry, Universidade Federal do Pampa, Uruguaiana, RS, Brazil. Electronic address: giuliawp@gmail.com.

Abstract

This study aimed to verify whether a prolonged exposure to low-level mercury promotes haemodynamic disorders and studied the reversibility of this vascular damage. Rats were divided into seven groups: three control groups received saline solution (im) for 30, 60 or 90 days; two groups received HgCl2 (im, first dose, 4.6μg/kg, subsequent doses 0.07μg/kg/day) for 30 or 60 days; two groups received HgCl2 for 30 or 60 days (im, same doses) followed by a 30-day washout period. Systolic blood pressure (SBP) was measured, along with analysis of vascular response to acetylcholine (ACh) and phenylephrine (Phe) in the absence and presence of endothelium, a nitric oxide (NO) synthase inhibitor, an NADPH oxidase inhibitor, superoxide dismutase, a non-selective cyclooxygenase (COX) inhibitor and an AT1 receptor blocker. Reactive oxygen species (ROS) levels and antioxidant power were measured in plasma. HgCl2 exposure for 30 and 60 days: a) reduced the endothelium-dependent relaxation; b) increased the Phe-induced contraction and the contribution of ROS, COX-derived vasoconstrictor prostanoids and angiotensin II acting on AT1 receptors to this response while the NO participation was reduced; c) increased the oxidative stress in plasma; d) increased the SBP only after 60 days of exposure. After the cessation of HgCl2 exposure, SBP, endothelium-dependent relaxation, Phe-induced contraction and the oxidative stress were normalised, despite the persistence of the increased COX-derived prostanoids. These results demonstrated that long-term HgCl2 exposure increases SBP as a consequence of vascular dysfunction; however, after HgCl2 removal from the environment the vascular function ameliorates.

KEYWORDS:

Blood pressure; Cessation of exposure; Long-term exposure; Mercury; Oxidative stress

PMID:
28222365
DOI:
10.1016/j.envres.2017.02.022
[Indexed for MEDLINE]

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