Hypertension is one of the most important contributors to atherosclerosis. A possible link between inflammation and elevated blood pressure has been suggested by several cross-sectional and longitudinal studies. Possible mechanisms include an imbalance between vasoconstrictors and vasodilators, amplified thrombogenesis and platelet activation, and perhaps a direct effect of inflammatory mediators. C-reactive protein (CRP), an inflammatory cytokine, may play an essential role in vascular inflammation and can directly decrease the production of nitric oxide, a vasocodilator. Angiotensin II (Ang II) up-regulates several inflammatory cytokines, leukocyte adhesion molecules, and chemokines through the activation of the nuclear factor-kappa B leading to a decrease in the bioavailability of vasodilators. The increase in oxidative stress and endothelin-1 production through Ang II may further contribute to vasoconstriction. Adipose tissue can add to the production of CRP and creates a prothrombotic state. The presence of low-grade inflammation, especially elevations of CRP, can help predict the risk of future cardiovascular events and is associated with target organ damage in hypertensive individuals. Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-adrenoreceptor antagonists, and, to a lesser degree calcium channel antagonists, have shown efficacy in reducing CRP. Lifestyle changes such as exercise, weight loss, and tobacco cessation have also shown a similar efficacy. Whether targeting inflammation in the treatment of uncomplicated hypertension can alter the natural history of the disease or lead to improved outcome has yet to be determined.