Figure 2.

Role of inflammation and immunity in hypertension. Many risk factors, such as genetic susceptibility, high salt, and environmental stress, can elevate blood pressure (BP) and consequently activate the sympathetic nerve system (SNS) or inhibit the parasympathetic nerve system (PNS). Over time, elevated BP can induce organ injury promoting the formation of damage-associated molecular patterns (DAMPs) and new antigens. In addition, several infectious diseases can enhance the activation of the innate immune system through the binding of pathogen-associated molecular patterns (PAMPs) to toll-like receptors. DAMPs, new antigens, and PAMPs activate innate immunity which interacts with adaptive immunity. Next, numerous proinflammatory cytokines are released and result in further organ injury. Through alternatively activated macrophages (M2) and Tregs have roles in anti-inflammatory response, the effect is too weak to reduce the organ damage. Finally, peripheral vascular resistance and blood volume increases to result in hypertension (Created with BioRender.com).