Scholarlink

<p>Mercury exposure is a significant environmental concern due to its toxic effects on the human body, especially on the cardiovascular system. Its accumulation induces oxidative stress, inflammation and endothelial dysfunction in systemic arteries, contributing to the development of cardiovascular diseases. The close relationship between systemic and pulmonary circulation leads us to believe that it must also suffer by the toxic effects of HgCl<sub>2</sub>. However, the consequences of HgCl<sub>2</sub> on pulmonary arteries remain unclear. This study aimed to investigate the effects of mercury chloride (HgCl₂) exposure for 60 d on the small intrapulmonary arteries and hemodynamic parameters of male rats. The rats were exposed to HgCl₂ (1st dose, 4.6&#xa0;μg/kg; subsequent daily doses, 0.07&#xa0;μg/kg; intramuscular injection). The results revealed that intrapulmonary arteries from exposed rats exhibited reduced contractile responses to potassium chloride and the thromboxane A2 receptor agonist U46619, along with thinning of the arterial wall, which is indicative of vascular remodeling. Impaired pulmonary vasoconstriction in the HgCl<sub>2</sub> group was associated with increased nitric oxide (NO) production and elevated hydrogen peroxide (H₂O₂) levels. In addition, increased production of superoxide anion (O<sub>2</sub><sup>•−</sup>) and reduced superoxide dismutase (SOD) expression were observed and indicates an environment of oxidative stress. Furthermore, HgCl<sub>2</sub> increased systemic blood pressure in conscious animals but reduced left ventricular systolic pressure in anesthetized animals. These findings suggest that chronic HgCl<sub>2</sub> exposure induces pulmonary vascular dysfunctions, primarily through enhanced NO and ROS signaling as an adaptive mechanism.</p> Graphical Abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Chronic Mercury Exposure Triggers Vascular Remodeling and Impaired Vasoconstriction in Small Intrapulmonary Arteries

  • 期刊论文

  • 发表日期：

    2025年8月13日

查看全文
  • Ingridy Reinholz Grafites Schereider,
  • Lorraine Christiny Costa Sepulchro Mulher,
  • Nina Bruna de Souza Mawandji,
  • Vanessa Cristina de Oliveira Souza,
  • Fernando Barbosa Junior,
  • Júlia Martins Vieira,
  • Maylla Ronacher Simões,
  • Dalton Valentim Vassallo

摘要

Mercury exposure is a significant environmental concern due to its toxic effects on the human body, especially on the cardiovascular system. Its accumulation induces oxidative stress, inflammation and endothelial dysfunction in systemic arteries, contributing to the development of cardiovascular diseases. The close relationship between systemic and pulmonary circulation leads us to believe that it must also suffer by the toxic effects of HgCl2. However, the consequences of HgCl2 on pulmonary arteries remain unclear. This study aimed to investigate the effects of mercury chloride (HgCl₂) exposure for 60 d on the small intrapulmonary arteries and hemodynamic parameters of male rats. The rats were exposed to HgCl₂ (1st dose, 4.6 μg/kg; subsequent daily doses, 0.07 μg/kg; intramuscular injection). The results revealed that intrapulmonary arteries from exposed rats exhibited reduced contractile responses to potassium chloride and the thromboxane A2 receptor agonist U46619, along with thinning of the arterial wall, which is indicative of vascular remodeling. Impaired pulmonary vasoconstriction in the HgCl2 group was associated with increased nitric oxide (NO) production and elevated hydrogen peroxide (H₂O₂) levels. In addition, increased production of superoxide anion (O2•−) and reduced superoxide dismutase (SOD) expression were observed and indicates an environment of oxidative stress. Furthermore, HgCl2 increased systemic blood pressure in conscious animals but reduced left ventricular systolic pressure in anesthetized animals. These findings suggest that chronic HgCl2 exposure induces pulmonary vascular dysfunctions, primarily through enhanced NO and ROS signaling as an adaptive mechanism.

Graphical Abstract