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Prolonged treatment with the at1receptor blocker, valsartan, increases small and large artery compliance in uncomplicated essential hypertension

Authors
Journal
American Journal of Hypertension
0895-7061
Publisher
Oxford University Press
Publication Date
Volume
15
Issue
12
Identifiers
DOI: 10.1016/s0895-7061(02)03134-5
Keywords
  • Original Contribution
Disciplines
  • Medicine

Abstract

Abstract Background Decreased arterial compliance (AC) is considered an early marker of vascular wall damage. Hypertension gradually decreases arterial compliance. We studied whether treatment with the angiotensin type 1 (AT 1) antagonist valsartan will affect AC in patients with essential hypertension (EH). Methods Twenty-two patients with EH, 6 men and 16 women, mean age 58.7 ± 4.1 years, without overt target organ damage were included. Antihypertensive medications were withdrawn for 3 weeks, Valsartan was given at 80- and 160-mg doses. The AC, blood pressure (BP), blood, and urine were measured monthly. Large (C1) and small (C2) AC were derived from radial artery waveforms, obtained using a calibrated tonometer (model CR-2000, HDI Inc., Eagan, MN). Results After 3 months, systolic BP decreased from 172 ± 17 to 142 ± 13 mm Hg ( P < .0001) and diastolic BP from 95 ± 9 to 82 ± 8 mm Hg ( P < .0001). The decrease in BP was significant within 1 month and improved further on. The C1 increased by 22%, from 8.0 ± 3.1 to 9.7 ± 2.3 mL/mm Hg × 10 ( P < .01). The C2 increased by 35%, from 2.9 ± 1.3 to 3.9 ± 1.9 mL/mm Hg × 100 ( P < .01). Both C1 and C2 reached statistical significance only after 3 months. Systemic vascular resistance (SVR) decreased by 15% from 2140 ± 376 to 1817 ± 262 dynes/sec/cm −5 ( P < .0001). Conclusions Treatment with valsartan in patients with EH improves small and large AC. The improvement in AC was significant only after 3 months of treatment, whereas systolic BP, diastolic BP, and SVR decreased earlier. The AT 1 receptor blockade with valsartan seems to be an effective means of not only lowering BP but of reversal of vascular wall damage, which predisposes to cardiovascular events.

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