The Cooperative Roles of Inflammation and Oxidative Stress in the Pathogenesis of Hypertension

Abstract

Innate and adaptive immunity play fundamental roles in the development of hypertension and its complications. As effectors of the cell-mediated immune response, myeloid cells and T lymphocytes protect the host organism from infection by attacking foreign intruders with bursts of reactive oxygen species (ROS). While these ROS may help to preserve the vascular tone and thereby protect against circulatory collapse in the face of overwhelming infection, aberrant elaboration of ROS triggered by immune cells in the absence of a hemodynamic insult can lead to pathologic increases in blood pressure. Conversely, misdirected oxidative stress in cardiovascular control organs, including the vasculature, the kidney, and the nervous system potentiates inflammatory responses, augmenting blood pressure elevation and inciting target organ damage. Inflammation and oxidative stress thereby act as cooperative and synergistic partners in the pathogenesis of hypertension. Pharmacologic interventions for hypertensive patients will need to exploit this robust bidirectional relationship between ROS generation and immune activation in cardiovascular control organs to maximize therapeutic benefit, while limiting off-target side effects.