Exposição crônica ao cloreto de mercúrio induz disfunção endotelial em aorta e acelera o desenvolvimento da hipertensão em SHR jovens

• Ano de defesa: 2019
• Autor(a) principal: Simões, Rakel Passos
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal do Espírito Santo; BR; Mestrado em Ciências Fisiológicas; Centro de Ciências da Saúde; UFES; Programa de Pós-Graduação em Ciências Fisiológicas
• Palavras-chave em Português: Mercury exposure; Vascular reactivity; Young SHR; Exposição por mercúrio; Reatividade vascular; Aorta; PGE2; SHR jovem; Óxido nítrico; Coração - Doenças; Mercúrio; Hipertensão; Fisiologia; 612
• Link de acesso: http://repositorio.ufes.br/handle/10/11295

Mercury is a heavy metal widely dispersed in nature and upon contact with the human body causes damage to the vessels and to the heart, promoting the development of cardiovascular diseases. Chronic exposure to mercury chloride (HgCl2) for 30 days does not change blood pressure in adult normotensive rats, however, it is unknown what would be the effects of this exposure on prehypertensive animals. Thus, we aimed to compare the effects of chronic exposure to HgCl2 in normotensive rats and young spontaneously hypertensive rats (SHR). Four-week-old Wistar and SHR were treated daily with HgCl2 (1st dose 4.6 μg/kg, subsequent dose 0.07 μg/kg/day, im, 30 days) or 0.9% saline. In young normotensive animals, mercury exposure did not change systolic blood pressure (SBP), vascular reactivity to phenylephrine, superoxide anion production and the COX-2 pathway. However, it abolished modulation of contraction of aortic rings by the prostacyclin receptor (IP). In SHR, exposure to HgCl2 accelerated the development of hypertension and increased vascular reactivity to phenylephrine, at least in part, by increasing the participation of the EP1 pathway and reducing IP pathway. In addition, HgCl2 increased oxidative stress, confirmed by higher in situ production of superoxide anion, and reduced the participation of antioxidant enzymes, corroborated with the decrease in SOD-1 protein levels in aorta. Together, these effects characterize endothelial dysfunction in SHR and this seems to be the reason why mercury accelerates the development of hypertension in these animals. These findings suggest that mercury exposure changes the natural course of hypertension in young SHR and is a cardiovascular risk factor for pre-hypertensive individuals.