Hypertension, obesity, and inflammation: the complex designs of a deadly trio

Abstract

Hypertension is a powerful risk factor for cardiovascular disease and frequently occurs in conjunction with obesity and the metabolic syndrome. Recent research into the underlying pathophysiologic processes common to these entities has uncovered the role of a heightened inflammatory state signified by a host of circulating biocytokines. Systemic and local hormonal effectors, such as angiotensin II and aldosterone, interact with inflammatory and oxidative stress to augment endothelial damage in a complex manner. The kidneys play a prominent role in the renin-angiotensin cascade and the abnormal pressor response that ensues. Insulin resistance underlies the pathogenesis of obesity and the metabolic syndrome. The interplay of hypertension, insulin resistance, and obesity vastly enhances the noxious influence of inflammation on the vasculature, promoting deleterious immune adaptations and ultimately increasing atherosclerotic risk. Although certain classes of available pharmacologic agents already address the altered endovascular and humoral dynamics in hypertension, a better understanding of the proinflammatory picture holds promise of targeted treatment modalities in future.