Resistance arteries as endpoints in hypertension

Abstract

Resistance arteries are small vessels measuring less than 400 microm which present alterations in their structure and function in hypertension. These alterations correlate with the severity of elevation of blood pressure, and include a smaller lumen which increases resistance to blood flow and an elevated media to lumen ratio, which may amplify responses to vasoconstrictors. The endothelium of these arteries has a reduced ability to induce vascular relaxation due to an impaired response or increased inactivation of endothelium-derived nitric oxide. As a consequence, these vessels may play a role in myocardial, cerebral and renal complications of hypertension. In humans study of these small vessels is mostly limited to indirect evaluations of their structure or function. Direct examination of these vessels has been performed in studies in which these arteries have been dissected from gluteal subcutaneous biopsies or from material obtained at surgery. Repeat gluteal subcutaneous biopsies have allowed the demonstration that some antihypertensive agents improve the structure and endothelium-dependent relaxation of these arteries in well-defined populations of hypertensive patients. These effects on gluteal subcutaneous small arteries and the changes initially present are similar to those found in more critical vascular beds in experimental hypertensive animals, and using indirect methods in the coronary circulation in humans. Although these apparently beneficial effects still remain to be correlated with hard endpoints (myocardial ischemic events, stroke, etc.), these results suggest that these small resistance arteries may serve as surrogate endpoints in hypertension.