Abstract

Although evidence from basic research suggests the involvement of angiotensin II (Ang II) in the progression of arteriosclerosis, the clinical data are limited. In the present study, hypertensive outpatients who were well controlled with antihypertensive medication and had similar blood pressure levels were studied, and arterial elasticity was compared between those receiving Ang II receptor blockers (ARBs) and those treated with other antihypertensive agents. The effects of HMG-CoA reductase inhibitors (STs) on arterial elasticity were also evaluated. The study enrolled 298 outpatients who had been diagnosed with essential hypertension whose blood pressure was controlled to 150/95 or less by antihypertensive treatment (excluding angiotensin converting enzyme [ACE] inhibitors) for at least 2 months. The small artery elasticity index (SAEI) was determined for each patient from the radial artery pulse waves using a non-invasive pulse wave analysis system CR-2000. The mean of two blood pressure measurements taken from subjects lying in a recumbent position during SAEI analysis was used for the data analysis. The patients were grouped according to the use of ARBs and STs, and two-way analysis of variance (ANOVA) was used for statistical comparisons. A backward stepwise multiple regression analysis was carried out to identify factors contributing to the SAEI. Hypertensive patients receiving ARB treatment had a significantly higher SAEI compared to those not receiving ARBs, despite the similar blood pressure levels of both groups. No significant effects of ST treatment on the SAEI were observed (two-way ANOVA). A backward stepwise multiple regression analysis for the SAEI suggested that ARB treatment was an independent determinant of the SAEI after the adjusting of age, gender, total cholesterol, high density lipoprotein cholesterol, smoking and systolic blood pressure. Our results suggested that while providing blood pressure control similar to that of other antihypertensive agents, ARBs may also increase vascular elasticity and thereby delay the progression of arteriosclerosis.

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