title: Prolonged treatment with the AT1 receptor blocker, valsartan, increases small and large artery compliance in uncomplicated essential hypertension.
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 Antihypertensive medications were withdrawn for 3 weeks, Valsartan was given at 80- and 160-mg doses.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 x 10 (P <.01). The C2 increased by 35%, from 2.9 +/- 1.3 to 3.9 +/- 1.9 mL/mm Hg x 100 (P <.01). Both C1 and C2 reached statistical significance only after 3 months. Systemic vascular resistance (SVR) decreased by 15% from 2,140 +/- 376 to 1,817 +/- 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.
authors.affiliation: Department of Endocrinology, Wolfson Medical Center, Holon, Israel.
authors.forename: Marina
authors.initials: M
authors.lastname: Shargorodsky
authors.forename: Eyal
authors.initials: E
authors.lastname: Leibovitz
authors.forename: Leonid
authors.initials: L
authors.lastname: Lubimov
authors.forename: Dov
authors.initials: D
authors.lastname: Gavish
authors.forename: Reuven
authors.initials: R
authors.lastname: Zimlichman
mesh_terms: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D004548:Elasticity / Q000187:drug effects; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D013777:Tetrazoles / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D016896:Treatment Outcome; D014633:Valine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology* / Q000627:therapeutic use; D000068756:Valsartan; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine