Vascular endothelial function and hypertension: insights and directions

Abstract

Hypertension contributes significantly to worldwide cardiovascular morbidity and mortality. Hypertension appears to have a complex association with endothelial dysfunction, a phenotypical alteration of the vascular endothelium that precedes the development of adverse cardiovascular events and portends future cardiovascular risk. This review concentrates on recent findings with respect to the mechanisms of hypertension-associated endothelial dysfunction, the interrelationship between these two entities, and the relationship of the efficacy of antihypertensive therapies to improvements in vascular homeostasis beyond blood pressure reduction. Current evidence suggests that hypertension and endothelial dysfunction are integrally related with respect to pathophysiologic mechanisms. Future studies will need to identify the key connections between hypertension and endothelial dysfunction to allow novel interventions to be designed and promulgated.

Fig. 1

Potential mechanism of hypertension-associated endothelial dysfunction. Recent publications suggest that hypertension is associated with increased production of reactive oxygen species (ROS) from mitochondria and NADPH oxidase in the vascular endothelium. Local and systemic inflammation also occurs, leading to an increase in activated complement factor 3 (C3) and subsequent increased vascular damage through reduced endothelial progenitor cell (EPC) activity and inflammation-related damage. The resultant excessive oxidative stress and inflammation result in endothelium-dependent vasomotor dysfunction. Endothelial dysfunction may subsequently worsen hypertension. CRP—C-reactive protein