Exposição por 30 dias ao cobre aumenta a pressão arterial e altera a contratilidade cardíaca: envolvimento do óxido nítrico e do estresse oxidativo

• Ano de defesa: 2020
• Autor(a) principal: Rozetti, Cindy Medici Toscano
• Orientador(a): Vassallo, Dalton Valentim
• Banca de defesa: Pires, Jose Guilherme Pinheiro , Simões, Maylla Ronacher , Santos, Leonardo dos , Wiggers, Giulia Alessandra
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal do Espírito Santo; Doutorado em Ciências Fisiológicas
• Programa de Pós-Graduação: Programa de Pós-Graduação em Ciências Fisiológicas
• Departamento: Centro de Ciências da Saúde
• País: BR
• Palavras-chave em Português: Cobre; Pressão arterial; Contratilidade cardíaca; Estresse oxidativo
• Área do conhecimento CNPq: Fisiologia
• Link de acesso: http://repositorio.ufes.br/handle/10/14638

Copper contributes as an essential element for the body homeostasis. However, copper excess can compromise organic functions, including the cardiovascular system. We investigated the effects of copper exposure for 30 days on blood pressure (BP) and cardiac contractility and the involvement of nitric oxide (NO) and reactive oxygen species (ROS). Wistar rats (12 weeks old, 280 g) were randomized to treated group (Cu) exposed to copper for 30 days (2000 μg/kg/day CuCl2) and control group (Ct) receiving intraperitoneal saline (0,9%). The Cu group presented increased blood copper concentration ~1,26 μg/mL and Ct ~0,024 μg/mL. Copper exposure increased systolic BP (Cu: 141 ± 3 mmHg; Ct: 133 ± 3 mmHg) (tail cuff) and arterial and intraventricular hemodynamic pressures. The sites with the highest accumulation of the metal were liver, kidneys and tibia in relation to the other organs analyzed in the present study. Copper increased the development of papillary muscle force and L-NAME did not alter this response. The sarcoplasmic reticulum appears to capture less calcium from the cytoplasm in the cardiomyocyte. The contractile response to Ca2+ was increased by copper and L-NAME potentiated this increase. Copper increased contractions dependent on the Ca2+ transarcolemal influx, but LNAME reduced the effect in both groups. The contractile response to isoproterenol was lower in the treated groups and L-NAME did not change this result. The force development of the papillary muscles at the peak and plateau of tetanus contractions increased after copper exposure, but without changes by L-NAME. In conclusion, 30 days of copper exposure increased the BP and the development of force of the cardiac papillary muscles, increased the influx of Ca2+ and slowed its reuptake by the RS, in which OH● and NO are involved. Thus, exposure to copper can be harmful and cause cardiovascular damage.