The vascular wall has the capacity to undergo remodeling in response to long-term changes or injuries. This is a process of structural rearrangement that involves cell growth, cell death, cell migration, cell modulation and secretion/degradation of extracellular matrix molecules. Vascular remodeling is an adaptive phenomenon, e.g. Glagov's compensatory enlargement in atherosclerosis, but it may grow into vascular diseases, such as hypertension, atherosclerosis, and coronary restenosis after angioplasty. Nowadays paradigms defining the cell biology of vascular diseases are the following: (i) the hypertensive vessel is characterized by hyperinnervation-associated medial thickening due to smooth muscle cell (SMC) hypertrophy/hyperplasia and increased extracellular matrix content, (ii) the atherosclerotic plaque is characterized by SMC/immune cells/increased extracellular matrix-containing intimal thickening, and (iii) the restenotic coronary artery is characterized by SMC/immune cells-containing neointimal thickening. The spontaneously hypertensive rats (SHR), the stroke-prone SHR (SHRSP), the genetically hypertensive (GH) rats, and other genetically hypertensive strains are widely used as a model of human essential hypertension. In this volume of Biomedical Reviews, Bell updates the knowledge about vascular wall neurotrophobiology in relation to the pathogenesis of hypertension in SHR and GH rats. Also, Kondo et al systematize the perivascular nerve-related SMC structural changes in the development of hypertension in SHR and SHRSP. The data presented in these reviews are evaluated mainly in terms of Levi-Montalcini's neurotrophic theory.
Biomedical Reviews 1996; 6: 5-10.
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