Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation. Role of adrenergic and nitrergic innervation

Clinical Science (2011) Immediate Publication, doi:10.1042/CS20110072 Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation. Role of adrenergic and nitrergic innervationJavier Blanco-Rivero, Lorena B Furieri, Dalton V Vassallo, Mercedes Salaíces and Gloria BalfagónFisiología, Facultad de Medicina. Universidad Autónoma de Madrid, Madrid, Madrid 28029, Spain. gloria.balfagon@uam.es

Objectives: We investigated the possible changes in rat mesenteric artery vascular innervation function caused by chronic exposure to low doses of mercuric chloride (HgCl2), as well as the mechanisms involved.

Methods: Rats were divided into two groups: control and HgCl2-treated rats (30 days, 1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg·day im). Vasomotor response to electrical field stimulation (EFS), noradrenaline (NA) and nitric oxide (NO) donor DEA-NO were studied, neuronal NO synthase (nNOS) and phosphorylated nNOS (P-nNOS) protein expression were analysed and NO, superoxide anions (O2.-) and NA releases were also determined.

Results: EFS-induced contraction was higher in the HgCl2-treated group. 1 mmol/L phentolamine decreased the response to EFS to a greater extent in HgCl2-treated rats. HgCl2 treatment increased vasoconstrictor response to exogenous NA and NA release. 0.1 mmol/L L-NAME increased the response to EFS in both experimental groups but the increase was greater in segments from control animals. HgCl2 treatment decreased NO release and increased O2.- production. Vasodilator response to DEA-NO was lower in HgCl2 animals. Tempol increased DEA-NO-induced relaxation to a greater extent in HgCl2-treated animals. nNOS expression was similar in arteries from both experimental groups, while P-nNOS was decreased in segments from HgCl2-treated animals.

Conclusion: HgCl2 treatment increased vasoconstrictor response to EFS as a result, at the least, of reduced NO bioavailability and increased adrenergic function. These findings offer further evidence that mercury, even at low concentrations, is an environmental risk factor for cardiovascular disease.

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