Various studies support the notion that inflammation contributes to endothelial dysfunction and the development of HTN.64 Systemic low-grade inflammation, as reflected by increased C-reactive protein (CRP) and cytokine levels, is thought to precede HTN.65 Immune cell function, particularly involving T cells and macrophages, has been directly implicated in the development of HTN in animal models, possibly by causing endothelial dysfunction as a consequence of cytokine-mediated alterations in the rates of synthesis and degradation of nitric oxide and other vasoconstrictors or vasodilators. Here, CRP is linked to hypertensive disorder.