Chronic mercury exposure at different concentrations produces opposed vascular responses in rat aorta

Abstract

Mercury chloride exposure for 30 days decreases NO bioavailability and increases oxidative stress. However, the mechanisms underlying the effects of mercury on the cardiovascular system are not completely understood, and it is not known if they are dose-dependent or if some concentrations have no harmful effects. Thus, we investigated the effects of chronic exposure to doses low (half) and high (2.5-fold higher) than that needed to obtain 29 nmol/L of HgCl2 on the vascular function. Three-month-old male Wistar rats received intramuscular (i.m.) HgCl2 for 30 days and were divided in three groups: lower (Low Hg); higher (High Hg); and saline was used as the control. High Hg exposure increased the contractile response to phenylephrine (PHE) in aortic rings, but Low Hg reduced it. The hyporesponsiveness in the Low Hg rats was blunted by endothelial denudation and NOS inhibition with l-NAME (100 μmol/L). The phosphorylated-eNOS/eNOS protein ratio increased in the aortas of Low Hg rats. In the High Hg group, endothelial denudation increased the PHE-induced contractions, while l-NAME had no effects and indomethacin (10 μmol/L), losartan (10 μmol/L) and apocynin (30 μmol/L) reduced this response. In the High Hg group, protein levels of the NADPH oxidase subunit gp91phox and cyclooxygenase-2 increased. Our results support previous suggestions that High Hg increases oxidative stress that might activate an inflammatory cascade and the renin-angiotensin system. However, very low Hg concentrations below the level considered safe still reduced vascular reactivity, suggesting the need for special attention to continuous exposure as a putative cause of increased cardiovascular risk.

Impaired participation of potassium channels and Na+/K+‐ATPase in vasodilatation due to reduced nitric oxide bioavailability in rats exposed to mercury

“…In addition to the reduced releasing/action of endothelial NO, increased local production of vasoconstrictors, such as angiotensin II and COX‐derived prostanoids, appears to contribute to the impaired vasodilatation observed in our model. These data reinforced previous studies showing that incubation with both angiotensin‐converting enzyme inhibitors or angiotensin 2 type‐1 receptor antagonists reduced vasoconstrictor hyper‐reactivity in mercury‐exposed rats . Similarly, smaller doses of mercury have previously been shown to increase COX expression in aorta homogenate and its participation in the vasoconstrictor responses .…”

“…The data presented here indicate that incubation with the scavenger tiron indeed restored vasorelaxation in the Hg group. Similarly, incubation with superoxide dismutase or tiron, and acute or chronic treatment with apocynin have all been shown to prevent the vasoconstrictor hyper‐reactivity of different arteries in rats exposed to HgCl 2 . Furthermore, mercury was also shown to reduce antioxidant defence, glutathione peroxidase levels, catalase levels and superoxide dismutase levels …”

Prophylactic effect of the aqueous extract of Pimpinella anisum on the behavior of Wistar rats exposed to mercury

“…Mercury is an environmental pollutant linked to a high health risk. Studies on this metal have shown that it can harm several systems such as: cardiovascular, respiratory, renal, nervous, reproductive and immune (Azevedo et al, 2016).…”

Mercury Biodistribution in Rats after Chronic Exposure to Mercury Chloride

“…In this regard, it has been identified harmful effects to the nervous, cardiovascular renal and other systems. 4,5,[9][10][11][12][13] About the distribution of mercury among the organs and tissues, it was demonstrated that once organic mercury is absorbed, it is almost totally oxidized to the divalent form (inorganic mercury) in erythrocytes, liver and kidneys.…”