Role of adventitia in vascular remodeling in hypertension: a trophobiological view
George N. Chaldakov, Kamen P. Valchanov, and Peter I. Ghenev ( Bulgaria )
The vascular wall has the capacity to undergo remodel- ing in response to long-term changes or injuries. This is a pro- cess of structural rearrangement that involves cell growth, cell death, cell migration, cell modulation and secretion /degrada- tion of extracellular matrix molecules (1). Vascular remodel- ing is an adaptive phenomenon, e.g. Glagov’s compensatory en- largement in atherosclerosis (2), but it may grow into vascular diseases (1), such as hypertension (3), atherosclerosis (4,5), and coronary restenosis after angioplasty (2,6, 7). Nowadays para- digms defining the cell biology of vascular diseases are the following: (i) the hypertensive vessel is characterized by hy- perinnervation-associated medial thickening due to smooth muscle cell (SMC) hypertrophy/hyperplasia and increased ex- tracellular matrix content, (i) the atherosclerotic plaque is characterized by SMC/immune cells/increased extracellular matrix-containing intimal thickening, and (Hi) the restenotic coronary artery is characterized by SMC/immune cells-contain- ing neointimal thickening. The spontaneously hypertensive rats (SHR), the stroke-prone SHR (SHRSP), the genetically hyper- tensive (GH) rats, and other genetically hypertensive strains are widely used as a model of human essential hypertension. In this volume of Biomedical Reviews , Bell (8) updates the knowledge about vascular wall neurotrophobiology in relation to the patho-
genesis of hypertension in SHR and GH rats. Also, Kondo et al (9) 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 Le vi-Montalcini’s neurotrophic theory (10).
Biomed Rev 1996; 6: 5-10.