title: Effects of valsartan and nifedipine coat-core on systemic arterial stiffness in hypertensive patients.
abstract: BACKGROUND
  The aim of this study was to compare the effects of long-term antihypertensive treatment on brachial-ankle pulse wave velocity (PWV), a marker of systemic arterial stiffness, between angiotensin II receptor blocker valsartan and long-acting calcium channel blocker nifedipine coat-core.
  
  
  METHODS
  Forty-one patients (54 +/- 3 years of age, 20 men and 21 women) with essential hypertension (155 +/- 3/95 +/- 3 mm Hg) were randomly allocated to the treatment with valsartan (80 mg once daily) or nifedipine coat-core (20 mg once daily). Brachial-ankle PWV and 24-h ambulatory blood pressures (BP) were measured before and 3 months after treatment.
  
  
  RESULTS
  Baseline data did not differ between the valsartan and nifedipine groups. The PWV also was similar between the groups (1669 +/- 65 v 1622 +/- 64 cm/sec). Three months of treatment similarly reduced resting systolic and diastolic BP (nifedipine, -18.4 +/- 4.2/-11.9 +/- 2.7 mm Hg; valsartan, - 17.4 +/- 3.3/-9.8 +/- 2.1 mm Hg, all P < .001). The PWV was significantly reduced compared with baseline values in the valsartan group (-195 +/- 42 cm/sec, P < 0.001) but not in the nifedipine group (-69 +/- 40 cm/sec, NS). The 24-h mean heart rate increased in the nifedipine group but remained unchanged in the valsartan group, although BP were similarly lowered for 24 h. A tachycardic response was associated with an increase or lesser reduction in PWV in a group treated with nifedipine (r = 0.584, P < .01).
  
  
  CONCLUSIONS
  These data suggest that long-term treatment with valsartan could reduce arterial stiffness better than nifedipine-coat core. The favorable vascular effect of valsartan was due in part to its nonhypotensive effect. The expected decrease in arterial stiffness may be offset by reflex sympathetic activation in some patients treated with nifedipine.
authors.affiliation: Preventive Medical Center, Tohoku Rosai Hospital, Sendai, Japan. munakata.@tohokuh.rofuku.go.jp
authors.forename: Masanori
authors.initials: M
authors.lastname: Munakata
authors.forename: Akio
authors.initials: A
authors.lastname: Nagasaki
authors.forename: Tohru
authors.initials: T
authors.lastname: Nunokawa
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Sakuma
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kato
authors.forename: Kaoru
authors.initials: K
authors.lastname: Yoshinaga
authors.forename: Takayoshi
authors.initials: T
authors.lastname: Toyota
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000187:drug effects; D018660:Blood Pressure Monitoring, Ambulatory; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000627:therapeutic use*; D013777:Tetrazoles / Q000627:therapeutic use*; D016896:Treatment Outcome; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine; D009543:Nifedipine