Hypertension

Abstract

In the last decade, the pathophysiology of microcirculation has become an actively developing field of hypertension research, which we have felt it useful to review. An exact definition of microcirculation is elusive. It is often taken morphologically, to encompass all of the blood vessels with a diameter <150 μm, that is, some small arteries, arterioles, capillaries, and venules,1 with the morphological distinction between small arteries and arterioles not entirely clear, because some2 but not all authors3 limit the concept of arteriole to vessels containing a single layer of smooth muscle cells. Functionally, it is usually accepted that the arterial side of the microcirculation composes most of the resistance vessels, meaning that the largest part of the pressure drop between large conduit arteries and veins takes place in this segment.2,4 The “resistance” property of small arteries and arterioles is intimately, although not exclusively, related to the prevalence of myogenic tone in these vessels.5,6 Myogenic tone is an intrinsic property of vascular smooth muscle, which contracts in response to stretching, independent of any nerve or humoral mediation.5 All arteries have myogenic tone and, therefore, contract in response to an increase in blood pressure. Myogenic tone gains in importance with decreasing vessel caliber,7,8 and only in small arteries and arterioles (diameter: 15 to 300 μm, depending on species and organ) can it provoke substantial luminal narrowing (or even closure) in reaction to an increase in transmural pressure.8,9 In the hamster cheek pouch, for example, control of arterial/arteriolar luminal size by myogenic tone seems minimal in the feeding saccular arteries (diameter 135 μm) but progressively more intense in the A1 (80 μm), A2 (40 μm), and A3 arterioles (28 μm).8 Myogenic tone serves a simple purpose: to protect the distal capillaries against deleterious local hypertension. …