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• W3124391808 abstract "• Mercury has been recognized as an environmental pollutant and nephrotoxic chemical. • Acute mercury infusion reduced RBF and GFR associated with increased RVR in rats. • HgCl 2 reduced NHE3 activity and increased the serine 552 phosphorylation of NHE3. • Isolated renal vascular bed increased pressure and impaired endothelial function. • HgCl 2 -induced renal damage should be, at least in part, due to vascular dysfunction. Mercury is an environmental pollutant and a threat to human health. Mercuric chloride (HgCl 2 )-induced acute renal failure has been described by several reports, but the mechanisms of renal dysfunction remain elusive. This study tested the hypothesis that HgCl 2 directly impairs renal vascular reactivity. Additionally, due to the mercury toxicity on the proximal tubule, we investigated whether the HgCl 2 -induced natriuresis is accompanied by inhibition of Na + /H + exchanger isoform-3 (NHE3). We found that 90-min HgCl 2 infusion (6.5 μg/kg i.v.) remarkably increased urinary output, reduced GFR and renal blood flow, and increased vascular resistance in rats. “In vitro” experiments of HgCl 2 infusion in isolated renal vascular bed demonstrated an elevation of perfusion pressure in a concentration- and time-dependent manner, associated with changes on the endothelium-dependent vasodilatation and the flow-pressure relationship. Moreover, by employing “in vivo” stationary microperfusion of the proximal tubule, we found that HgCl 2 inhibits NHE3 activity and increases the phosphorylation of NHE3 at serine 552 in the renal cortex, in line with the HgCl 2 -induced diuresis. Changes in renal proximal tubular function induced by HgCl 2 were parallel to increased urinary markers of proximal tubular injury. Besides, atomic spectrometry showed that mercury accumulated in the renal cortex. We conclude that acute HgCl 2 exposure causes renal vasoconstriction that is associated with reduced endothelial vasodilator agonist- and flow-mediated responses and inhibition of NHE3-mediated sodium reabsorption. Thus, our data suggest that HgCl 2 -induced acute renal failure may be attributable at least in part by its direct effects on renal hemodynamics and NHE3 activity." @default.
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• W3124391808 date "2021-05-01" @default.
• W3124391808 modified "2023-10-14" @default.
• W3124391808 title "Changes in the renal function after acute mercuric chloride exposure in the rat are associated with renal vascular endothelial dysfunction and proximal tubule NHE3 inhibition" @default.
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• W3124391808 doi "https://doi.org/10.1016/j.toxlet.2021.01.014" @default.
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