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

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.