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Epidemiological and clinical studies have shown that cardiovascular disease in patients with end-stage renal disease (ESRD) is frequently related to damage of large conduit arteries. Arterial disease is responsible for the high incidence of ischaemic heart disease, peripheral artery diseases, left ventricular hypertrophy and congestive heart failure. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischaemic lesions being the most characteristic consequence, the latter primarily disturbs the dampening function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and wall hypertrophy of large conduit arteries and stiffening of arterial walls. These changes represent a clinical form of an accelerated ageing process. The main clinical characteristics due to arterial stiffening are isolated increase in systolic blood pressure with normal or lower diastolic pressure resulting in an increased pulse pressure. The consequences of these alterations are: (i) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; and (ii) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodelling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients. [ABSTRACT FROM AUTHOR]

1. In arterial hypertension, aortic wave reflections contribute to determining central systolic and pulse pressures. The present study assessed the central pressure alterations at the level of the common carotid artery following 1 month treatment with perindopril or atenolol and investigated during the 8 h following drug intake. 2. Twenty patients suffering from permanent hypertension were included after a 4 week run-in placebo period in a double-blind, randomized cross-over study comparing the angiotensin-converting enzyme (ACE) inhibitor perindopril with the beta-blocker atenolol during a 4 week treatment period. 3. Before and during the 8 h after drug intake, serial measurements included brachial artery systolic and diastolic blood pressures (SBP and DBP, respectively; mercury sphygmomanometer), carotid artery SBP and pulse pressure (PP; applanation tonometry), aortic pulse wave velocity (Complior; Colson, Les Lilas, France) and arterial wave reflections from the aorta (applanation tonometry; Sphygmocor; PWV Medical, Sydney, NSW, Australia). 4. Both treatments decreased brachial and carotid artery SBP, DBP and PP. Heart rate and pulse wave velocity decreased following atenolol (P < 0.001). Pulse wave velocity was reduced slightly following perindopril (NS). Arterial wave reflections were significantly (P < 0.001) decreased with perindopril in comparison with atenolol, but this effect on wave reflections was not associated with a larger decrease in carotid artery PP. 5. Thus, during chronic treatment, ACE inhibition and selective beta1-adrenoceptor blockade resulted in a similar decrease in brachial and carotid artery PP, but only atenolol reduced heart rate. Aortic pulse wave velocity was reduced with both drugs, but atenolol appeared more effective in improving aortic stiffness. Arterial wave reflections were decreased only following perindopril. 6. Central pulse pressure was improved following 1 month treatment with an ACE inhibitor or beta-adrenoceptor blockade following a decrease in arterial wave reflections with perindopril and a higher decrease in regional aortic stiffness with atenolol.