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

Abstract

Mercury intoxication is a public health risk factor due to its hazardous effect to several organs, including the cardiovascular system. There is evidence of endothelial dysfunction after exposure to mercury, but the effects on endothelium-dependent vasodilatation are still unknown. In the present study, we aimed to evaluate the chronic effects of high HgCl doses on the mechanisms of vasodilatation. Wistar rats were injected with HgCl (1st dose 10.86 μg/kg, and daily doses 0.014 μg/kg for 30 days i.m.), and saline was used as control. Mercury exposure reduced the acetylcholine-induced vasodilatation in aortic rings, which was restored by incubation with antioxidant tiron. Inhibition of the NO synthase, Na /K -ATPase and K channels indicates reduced participation of these factors. In the mercury group, there were an increased local anion superoxide and a reduced NO. The vasodilatation to exogenous NO was partially inhibited by co-incubation with TEA plus tiron, suggesting that reduced NO bioavailability is the responsible to that decreased the participation of K channels. Moreover, there was an increased participation of the Na /K -ATPase associated with an up-regulation of its alpha-1 subunit. In conclusion, reduced NO bioavailability plays a major role in the impaired participation of K channels and Na /K -ATPase in the acetylcholine-mediated relaxation, although sodium pump is up-regulated probably as a compensatory mechanism.

Antioxidant Properties of Egg White Hydrolysate Prevent Mercury-Induced Vascular Damage in Resistance Arteries

“…It has been previously reported that alterations in eNOS gene increase the susceptibility to cardiovascular diseases in individuals after Hg exposure by modulating NO levels ( de Marco et al, 2012 ). Exposure to Hg at low concentrations has deleterious vascular effects on aorta, coronary and basilar arteries related to greater vascular reactivity caused by the reduction of NO bioavailability in these vessels ( Wiggers et al, 2008 ; Peçanha et al, 2010 ; Botelho et al, 2019 ). Moreover, a study in mesenteric arteries from rats exposed for 30 days to HgCl 2 showed eNOS protein expression upregulation possibly due to a compensatory mechanism against metal-induced endothelial dysfunction ( Wiggers et al, 2008 ).…”

Paracetamol‐induced metabolic and cardiovascular changes are prevented by exercise training

“…Treatment with antioxidant compounds (including tiron and vitamin C) has proved effective in re-establishing blood vessel dilatation in environments of high oxidative stress. 15,42 Vascular GSH levels were determined to ascertain whether there were differences in its depletion in the trained or sedentary rats after PAR exposure. Some studies have shown an increase in lipid peroxidation and a decrease in GSH in the blood and target organs like the kidney and liver of PAR-treated rats.…”

“…Here, in order to confirm if decreased relaxation after PAR treatment is mediated by increased oxidative stress, isolated arteries were treated with antioxidant tiron, which normalized the relaxation response to both ACh and SNP. Treatment with antioxidant compounds (including tiron and vitamin C) has proved effective in re‐establishing blood vessel dilatation in environments of high oxidative stress 15,42 …”

Differential vasodilator effect of Dioclea rostrata lectin in conductance and resistance arteries: Mechanisms and glycoconjugate binding relationships

“…The reactivity assay for thoracic aorta was performed as detailed elsewhere 19 . The artery was divided into cylindrical segments of 4 mm in length and vertically mounted in organ baths for large vessels containing modified Krebs‐Henseleit solution (in mmol/L: NaCl 127; KCl 4.7; CaCl 2 .2H 2 O 2.5; MgSO 4 .7H 2 O 1.2; KH 2 PO 4 1.17; NaHCO 3 24; Glucose 5 and EDTA 0.01) heated to 36 ± 0.5ºC and aerated with 95% O 2 and 5% CO 2 , keeping the pH at 7.4.…”