This review describes the adaptive response of the vascular wall to a chronic increased load, that is, increased transmural pressure. Because it is not clear whether the changes in the vascular wall in various animal models of systemic or pulmonary arterial hypertension are due solely to an increase in transmural pressure, this review concentrates on experimental models in which increased pressure is the primary stimulus. This restriction means that the great majority of experiments discussed were performed on conduit vessels. Currently, there is insufficient evidence to determine whether changes observed in conduit vessels also occur in microvessels. Vascular heterogeneity is well docu mented; therefore, it would not be surprising to find that microvessels respond differently than conduit vessels. This review covers the following models of increased load: vessel coarctation, venous-to-arterial autologous grafts, and stretched, in vitro preparations of vessel wall or cultured vascular smooth muscle cells. The known morphological, protein, and functional changes correlated with an increase in load are discussed. We must begin with a description of morphological, protein, and functional changes in normal vascular smooth muscle because they change over the course of development. Any increase in load is applied to this changing base line; therefore, the characteristics of the vascular response to a given load vary with the age of the animal at the time of onset.
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Seidel et al. (1987) studied this question.
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