Large artery structure and function in hypertension and end-stage renal disease.

The cardiovascular complications in hypertension are ascribed to two different but associated alterations, namely atherosclerosis and arteriosclerosis. Whereas the former disturbs principally the conduit function and the delivery of an adequate blood flow to peripheral organs and tissues, the latter disturbs the cushioning function of large arteries, inducing an inadequate increase in systolic and pulse pressure. Arteriosclerosis represents a clinical form of accelerated ageing process and is characterized by a diffuse dilation and hypertrophy of large conduit arteries and stiffening of arterial walls. Independently from the ageing, structural changes are associated with several haemodynamic alterations such as increased in blood flow and flow velocity, and increased parietal stress due to increased arterial diameters and/or intraarterial pressure. The principal consequences of arterial stiffening are: (1) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; (2) altered coronary perfusion and blood flow distribution; and (3) decreased perfusion reserve during haemodynamic stress. In the absence of controlled studies, it is difficult to propose therapeutic interventions aimed to prevent or treat arterial abnormalities in hypertensive patients. It has been shown that long-term administration of either calcium channel blockers and angiotensin converting enzyme inhibitors led to an improvement of vessel wall elasticity. Nevertheless, these studies did not conclude whether the improvement of elastic properties were due only to decrease in blood pressure or to alterations in intrinsic properties of arterial walls. More investigations should be necessary to investigate this important problem.