title: Blood pressure lowering with valsartan is associated with maintenance of cerebral blood flow and cerebral perfusion reserve in hypertensive patients with cerebral small vessel disease.
abstract: BACKGROUND
  The purpose of this study was to determine the effect of systemic blood pressure-lowering treatment with an angiotensin II receptor blocker, valsartan, on cerebral hemodynamics in patients with hypertension and evidence of cerebral small vessel disease.
  
  
  METHODS
  We used positron emission tomography and acetazolamide challenge tests to measure cerebral blood flow (CBF) and cerebrovascular reserve (CVR) in 8 patients with hypertension (mean age 70.8 years) with lacunar infarcts and white matter lesions before and after valsartan therapy.
  
  
  RESULTS
  Systemic blood pressure was significantly decreased from baseline after treatment with valsartan. The baseline global CBFs before and after treatment were 38.2 +/- 5.6 mL/min/100 g and 39.9 +/- 9.0 mL/min/100 g, respectively. The CVRs before and after treatment were 52.2 +/- 18.4% and 39.7 +/- 18.9%, respectively. Differences in these parameters were not significant. Both regional CBF and CVR in the corona radiata with moderate or severe white matter lesions were also preserved after valsartan therapy compared with those before treatment.
  
  
  CONCLUSIONS
  Cerebral hemodynamics were preserved after blood pressure lowering with valsartan therapy. Valsartan could be a feasible antihypertensive regimen in terms of cerebral circulation in patients with cerebral small vessel disease.
authors.affiliation: Department of Tracer Kinetics and Nuclear Medicine, Osaka University Graduate School of Medicine, Suita City, Osaka, Japan.
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Kimura
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kitagawa
authors.forename: Naohiko
authors.initials: N
authors.lastname: Oku
authors.forename: Katsufumi
authors.initials: K
authors.lastname: Kajimoto
authors.forename: Hiroki
authors.initials: H
authors.lastname: Kato
authors.forename: Makiko
authors.initials: M
authors.lastname: Tanaka
authors.forename: Manabu
authors.initials: M
authors.lastname: Sakaguchi
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Hougaku
authors.forename: Saburo
authors.initials: S
authors.lastname: Sakoda
authors.forename: Jun
authors.initials: J
authors.lastname: Hatazawa
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology; D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D002536:Cerebral Arteries / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology; D004232:Diuretics / Q000494:pharmacology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D002537:Intracranial Arteriosclerosis / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D008875:Middle Aged; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D049268:Positron-Emission Tomography; D013777:Tetrazoles / Q000494:pharmacology*; D016896:Treatment Outcome; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D004232:Diuretics; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine; D000086:Acetazolamide