PATHOPHYSIOLOGY OF ARTERIAL REMODELING IN HYPERTENSION

In recent years, arterial remodeling emerged as a key concept for the understanding of the pathogenesis of arterial hypertension, with numer ous pharmacological applications. The concept of ''remodeling'', advan ced by Baumbach and Heistad in 1988, states that, during hypertension, the structural changes in the resistance vessels may not be associate d with net growth. Experiments in genetically hypertensive rats and es sential hypertensive patients have shown that the increase in arteriol ar resistance to blood flow is due to structural changes which can be described not by net growth but by a process or rearrangement of other wise normal material. Later, the term ''vascular remodeling'' was used by Gibbons and Dzau (1994) to describe any 4 ''active process of stru ctural alteration that involves changes in at least four cellular proc ess - cell growth, cell death, cell migration, and production of extra -cellular matrix - and is dependent on a dynamic interaction between l ocally generated growth factors, vasoactive substances, and hemodynami c stimuli''. Remodeling may thus contribute to the pathophysiology of various large and small artery diseases including not only hypertensio n but also heart failure, atherosclerosis, restenosis after angioplast y, and pulmonary hypertension. The present review will discuss the ult rastructural and geometrical changes in large and small arteries of hy pertensive humans and animals, described as ''remodeling'', and their functional consequences, both at the site of conducting arteries (pote ntiation of atherosclerosis and autoregulation of arterial compliance) and resistive arteries (structural increase in peripheral vascular re sistance, hyperreactivity to arteriolar stimuli, decrease in the perfu sion reserve of target organs, and modifications of the autoregulation of regional blood flow).