What is the Evidence That Microcirculatory Dysfunction Can Contribute to Hypertension

The established phase of human essential hypertension is characterized by a normal cardiac output and an elevation in peripheral vascular resistance. Peripheral vascular resistance is dictated primarily by resistance across vessels between 10 and 300 ^m in luminal diameter, and the increase in total peripheral vascular resistance in essential hypertension is, therefore, likely to reflect changes in these vessels. Changes in the microcirculation of hypertensive patients include a reduction in the number of capillaries and arterioles, so-called rarefaction, in many tissues (41,50). Microvascular rarefaction, similar in magnitude to the rarefaction observed in patients with established hypertension, can already be demonstrated in subjects with mild hypertension, and in normotensive subjects with a genetic predisposition to high blood pressure. This suggests that rarefaction is not solely secondary to sustained elevation of blood pressure, but may precede and thus be a causal component of high blood pressure. Indeed, capillary rarefaction in muscle has been shown to predict the increase in mean arterial pressure over two decades (51). In addition, a smaller retinal arteriolar diameter has been shown to predict the occurrence and development of hypertension in a prospective, population-based study of normotensive middle-aged persons (52). Calculations by mathematical modeling of in vivo microvascular networks predict an exponential relationship between capillary and arteriolar number, and vascular resistance (41). Total vessel rarefaction up to 42% (within the range observed in hypertensive humans) can increase tissue vascular resistance by 21%. Thus, as seems likely, microvascular abnormalities can both result from and contribute to hypertension, and a "vicious cycle" may exist in which the microcirculation maintains or amplifies an initial increase in blood pressure. Because, according to the Borst-Guyton concept, chronic hypertension can occur only if renal function is abnormal, with a shift in the renal pressure-natriuresis relationship, subtle renal microvascular disease as well as a reduced number of nephrons (53) may reconcile the Borst-Guyton concept with the putative role of vessel rarefaction in the etiology of high blood pressure. This may also explain the relationship between salt sensitivity of blood pressure and insulin resistance (53).

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