Cada vez mais evidências apontam para um papel importante do estresse oxidativo no desenvolvimento da hipertensão arterial. Neste trabalho pudemos fornecer novas informações a respeito dos mecanismos envolvidos no desenvolvimento desta patologia, caracterizando as possíveis fontes do aumento da geração de EROs na vasculatura, como a Nox1, bem como diferenciando alterações importantes em arteríolas de resistência e artérias de condutância. Entendemos que o controle eficiente do aumento da PA através de diferentes terapias antihipertensivas em animais SHR, foi importante para inibir o aumento da geração de EROs e de Nox4 mesmo que, curiosamente, somente o tratamento com Losartan, antagonista de receptor AT1, tenha promovido uma diminuição na expressão de Nox1 em animais SHR. Adicionalmente o presente estudo abre a perspectiva da participação da PDI na modulação da geração de EROs pela Nox1 e sua contribuição para alterações na estrutura e função vascular mediadas pela Ang II em artérias de resistência durante o desenvolvimento da hipertensão arterial. Neste âmbito, tais resultados figuram-se importantes e abrem uma nova frente para investigação de um novo papel para a PDI, uma proteína com uma função primária no enovelamento proteico no retículo endoplasmático, na regulação de um fenômeno tão diferenciado como o aumento da geração de EROs e na disfunção vascular associada a patologias como hipertensão arterial.
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