Efeitos da exposição crônica ao cloreto de mercúrio sobre os mecanismos de vasodilatação da aorta de ratos

• Autor(a) principal: Nascimento, Tatiani Botelho
• Data de Publicação: 2016
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/7885
• topic: Mercury; Aortic; Vascular reactivity; Endotelial; Potassium channel; Reatividade vascular; Canais para potássio; Fisiologia; Mercúrio; Aorta; Reatividade (Química); Endotélio vascular; Potássio; 612

It is suggested that chronic exposure to mercury chloride (HgCl2) causes endothelial dysfunction associated with increased vasoconstriction due to reactive oxygen species (ROS) and reduced nitric oxide (NO) bioavailability. Thus, HgCl2- exposed people are at increased risk of developing cardiovascular disease. NO induces vasodilatation by different pathways, and little is known about the participation of potassium channels and Na+K + ATPase for mercury intoxication. The objective of this study was to evaluate the chronic effects of high doses of HgCl2 in the vasodilatation dependent on activation of some hyperpolarizing factors derived from the endothelium. Methods: Wistar rats were divided into control (CT, saline i.m.); HgCl2 (1st dose 10.86 mg/kg daily, and subsequent doses of 0.014 mg/kg for 30 days i.m.). Vascular reactivity of aortic segments to acetylcholine and sodium nitroprusside were evaluated in the presence of L-NAME, tiron, indomethacin, enalapril, ouabain, TEA, 4-aminopyridine, iberiotoxin or apamin. Exposure to HgCl2 reduced the endothelium-dependent vasodilatation. This alteration involves a reduction of the bioavailability of NO associated with increased ROS, increased ACE activity and probably COX pathway prostanoids. Furthermore, it was suggested that the reduction of NO decreases activation of BKCa and SKCa potassium channels. Similarly, reduced NO was responsible for the impaired activation of Na+K + ATPase during ACh-induced relaxation, although there was an increased expression of its α-subunit, indicating a compensatory mechanism. These observations reinforce further evidence that chronic mercury exposure is deleterious to the vascular function. We believe that the understanding of the mechanisms of the impaired vasodilatation should allow the development of new approaches for diagnosis and cardiovascular risk stratification, as well as future researches aimed at therapeutic interventions in mercury intoxication.