Microvascular Rarefaction

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Rarefaction in the microcirculation of hypertensives has been encounntered in patients and in experimental models with hypertension (Hutchins and Darnell, 1974). Functional rarefaction and structural rarefaction can be observed (Pre-witt et al., 1982). Functional rarefaction refers to a condition in which no or few blood cells are present in a microvessel due to a state of high vascular tone, but blood cells can be readily reintroduced by application of a vasodilator. Structural rarefaction refers to the physical loss of intact microvessel.

Functional Rarefaction and Blood Cell Distribution

Capillary networks, which are supplied by arterioles under high levels of vascular tone, exhibit functional rarefaction. The tone in arterioles is due in large part to smooth muscle contraction, which in small arterioles is also associated with deformation and folding of the endothelial cell. In terminal arterioles, a high tone may reach the point of complete lumen closure. Vascular tone is defined as

{steady state diameter minus the dilated diameter}/ {dilated diameter}.

The dilated diameter is measured after application of a saturating dose of vasodilators, such as papaverine or adenosine.

The average tone in arterioles of hypertensives is enhanced, leading to a reduction of blood flow from the arcade arterioles into terminal arterioles. At a divergent bifurcation from an arcade to a terminal arteriole, erythro-cytes and leukocytes enter preferentially into the vessels with the higher flow rates, i.e. terminal arterioles with enhanced microvascular tone receive a lower fraction of blood flow and therefore also a lower fraction of the blood cells. Therefore, if a terminal arteriole is constricted to the point at which no erythrocytes or leukocytes and only plasma and sporadic platelets enter, its downstream capillaries are filled mostly with plasma and exhibit functional rarefaction. Dilation of the terminal arteriole raises the blood flow and restores the flow of blood cells back into the capillary network. Thus functional rarefaction represents a redistribution of the microhematocit in the smallest microvessels and is reversible.

Structural Rarefaction and Endothelial Apoptosis

In contrast, structural rarefaction is not readily reversible by application of a vasodilator. Recent evidence in several forms of hypertension suggests that loss of capillaries is due to endothelial cell apoptosis (Vogt and Schmid-Schonbein, 2001).

Endothelial apoptosis may be detected in most segments of the circulation in hypertensives. In larger arterioles or venules with multiple endothelial cells along the wall perimeter, apoptosis of individual endothelial cells leads to a temporary shift in local endothelial permeability. In contrast, apoptosis of endothelial cells in true capillaries leads to actual loss of the microvessels since their wall is made up of single endothelial cells. The mesentery microcirculation of the SHR and WKY rats is subject to a non-uniform pattern of cell death, and is enhanced in selected microvascular segments by a glucocorticoid driven mechanism. Apoptosis is present in arterioles but also in capillaries and venules without elevated blood pressure. Enhanced apoptotic activity has been reported in every hypertensive model investigated to date, including the SHR, glucocorticoid-mediated hypertensives, and one kidney/one clip Goldblatt hypertensives. Apoptotic activity is observed in the kidney, heart, smooth and skeletal muscle, mesentery, and in the thymus and can be detected before blood pressure is elevated.

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