The biological behaviors of smooth muscle cells above-mentioned are triggered by the activated renin-angiotensin system and reactive oxygen species.[30–32] Secondly, studies have also indicated that the essential role of UA in arterial stiffness before the development of hypertension may be attributed to the activation of inflammatory pathways (increased levels of C-reactive protein and other proinflammatory factors).[33] Thirdly, UA has also been implicated in endothelial cell dysfunction, which plays a crucial role in arterial stiffening. Here, CRP is linked to hypertensive disorder.