title: Effects of angiotensin II receptor blockade with valsartan on pro-inflammatory cytokines in patients with essential hypertension.
abstract: Chronic inflammation is common in hypertension and acts as an independent determinant of arterial blood pressure. Hypertensive patients are reported to have high circulating levels of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and C-reactive protein (CRP). Recently, angiotensin II receptor blockers (ARBs) have been shown to possess benefits in addition to their ability to lower blood pressure, including anti-inflammatory and antioxidative properties within the vasculature. We evaluated the effects of the angiotensin II receptor blocker, valsartan, on these inflammatory cytokines. Thirty-nine patients with essential hypertension participated. These subjects received valsartan, 40 to 80 mg/day. Serum TNF-alpha, IL-6, CRP, and serum amyloid A (SAA) were measured before and after 3 months of treatment with valsartan. Valsartan significantly decreased systolic and diastolic blood pressure (160 +/- 16/92 +/- 11 mm Hg to 147 +/- 21/84 +/- 11 mm Hg, P = 0.001/P = 0.001, respectively). Serum TNF-alpha (9.1 +/- 8.6 pg/mL to 6.1 +/- 1.0 pg/mL, P = 0.006) and IL-6 (9.3 +/- 1.7 pg/mL to 8.9 +/- 1.4 pg/mL, P = 0.005) were significantly reduced after treatment with valsartan. However, C-reactive protein and serum amyloid A did not change. The angiotensin II receptor blocker, valsartan, may inhibit the development of atherosclerosis by lowering serum pro-inflammatory cytokines.
authors.affiliation: Second Department of Internal Medicine, National University Corporation, Ehime University, Toon City, Ehime, Japan.
authors.forename: Seiko
authors.initials: S
authors.lastname: Manabe
authors.forename: Takafumi
authors.initials: T
authors.lastname: Okura
authors.forename: Sanae
authors.initials: S
authors.lastname: Watanabe
authors.forename: Tomikazu
authors.initials: T
authors.lastname: Fukuoka
authors.forename: Jitsuo
authors.initials: J
authors.lastname: Higaki
mesh_terms: D000328:Adult; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002097:C-Reactive Protein / Q000032:analysis; D016207:Cytokines / Q000097:blood*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000276:immunology; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000032:analysis; D013777:Tetrazoles / Q000494:pharmacology* / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D016207:Cytokines; D015850:Interleukin-6; D000685:Serum Amyloid A Protein; D013777:Tetrazoles; D014409:Tumor Necrosis Factor-alpha; D000068756:Valsartan; D002097:C-Reactive Protein; D014633:Valine