IL-17A also regulates sodium transport in the kidneys, influencing natriuresis and blood pressure (129), contributing to endothelial dysfunction via the phosphorylation of the endothelial nitric oxide synthase (eNOS) (130), supporting the hypothesis that IL-17A plays a pathogenic role in the inflammation related to renal hypertension (Figure 2H). Here, NOS3 is linked to endothelial dysfunction.