Microcirculation and arterial hypertension.
A large part of the pressure gradient takes place in the microvascular network (which corresponds to vessels less than 150 microns in diameter). Most of the changes in the peripheral resistance associated with hypertension affect the microvascular network. From the brief review presented here, it appears that the functional characteristics of arterioles are significantly modified in hypertension. Sensitivity to numerous vasoconstrictive substances is increased. Local ACE activity is considerably higher, and endothelium-dependent dilation is lower, in genetically hypertensive animals than in control models. The myogenic response, which represents the vasoconstriction of arterioles in response to a stepped increase in pressure, is also amplified by mechanisms dependent on both prostanoids and endothelin. Changes also affect the structure of the microvascular network. Morphological alterations in the arteriolar wall are not observed for all types of hypertension. Conversely, arteriolar and capillary rarefaction appears to be the most commonly observed change affecting the structure of the microvascular network. The first stage of rarefaction is functional and affects the number of vessels perfused but not the total number of vessels of the microvascular network. At this stage, potent dilators can induce a recruitment of microvessels, which may cancel the difference between the number of perfused vessels in hypertensive and normotensive animals. The second stage is the anatomical rarefaction corresponding to a decrease in arterioles and/or the total number or density of capillaries. Microvascular rarefaction has also been described in patients even in the early stages of hypertension. This led us to consider the microvascular network not only as one of the putative factors responsible for increased pressure but also as a key target of hypertension. Consequently, antihypertensive drugs should also be assessed and differentiated in terms of their efficacy in preventing or reversing the microcirculatory damage associated with hypertension.
Vicaut
E
E
Laboratory for the Study of Microcirculation, F. Widal Hospital, Paris, France.
D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D008833:Microcirculation / Q000473:pathology / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000378:metabolism; D014665:Vasodilator Agents / Q000378:metabolism
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide; D007703:Peptidyl-Dipeptidase A