Microvascular Rarefaction in Hypertension—Reversal or Over-Correction by Treatment?

The microcirculation in hypertension is characterized by substantial structural and functional changes. The most consistent finding at the level of the microcirculation in individuals with primary hypertension is the smaller number of arterioles and capillaries compared with those of normotensive control subjects. This phenomenon, known as rarefaction, is a more steadily observed abnormality than a decrease in the arteriolar diameter in primary hypertension.1 Several mechanisms have been proposed to explain microvascular rarefaction; but recent research has suggested that capillary rarefaction in essential hypertension is likely to be a primary or a very early structural abnormality. In other words, rarefaction is thought to be a cause rather than a consequence of sustained hypertension, and it results from the anatomical absence of capillaries rather than functional nonperfusion. Several studies have shown that individuals predisposed to develop essential hypertension have significant rarefaction of their skin capillaries at basal conditions (ie, functional density) and also after maximization with reactive hyperemia or venous congestion (ie, structural density) reflecting a decreased angiogenic capacity of the microcirculation of individuals predisposed to hypertension.2