In addition to structural narrowing and increased wall thickness, a decrease in the number of arterioles and capillaries (rarefaction) has been widely reported in many different animal models of hypertension and in hypertensive humans. Microvessel rarefaction has two components: functional rarefaction, mediated by active closure of arterioles, and anatomical or structural rarefaction, mediated by an actual reduction in the number of arterioles. Several lines of evidence suggest that functional rarefaction can eventually progress to anatomical rarefaction. Microvascular rarefaction involves both the capillaries and the smaller (third- and fourth-order) arterioles and is accompanied by structural changes in the microvessels. Mathematical models suggest that microvessel rarefaction can have substantial effects on the microcirculation, including an elevation in vascular resistance (especially in conjunction with the constriction of arterioles) and a reduction in tissue Po2. The latter changes may be particularly significant in contributing to tissue damage under conditions of reduced perfusion. One interesting observation regarding microvessel rarefaction in salt-dependent forms of hypertension is that it has also been demonstrated to occur in normotensive animals on a highsalt diet. Arteriolar rarefaction in salt-dependent hypertension forms of hypertension and with high-salt diet in normotensive animals develops very rapidly and appears to be mediated by the angiotensin II (ANG II) suppression that occurs in response to elevated salt intake, since it can be prevented by continuous intravenous (i.v.) infusion of a low dose of ANG II to maintain normal circulating levels of ANG II without increasing blood pressure.
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