Angiotensin II–induced oxidative burst is fluvastatin sensitive in neutrophils of patients with hypercholesterolemia

• Published in: Metabolism, clinical and experimental Vol. 54; no. 9; pp. 1147 - 1154
• Main Authors: Seres, Ildiko, Fóris, Gabriella, Páll, Dénes, Kosztáczky, Béla, Paragh, Gyorgy, Varga, Zsuzsa
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.09.2005; Elsevier
• Subjects: Aged; Angiotensin II - pharmacology; Biological and medical sciences; Calcium - metabolism; Cells, Cultured; Disorders of blood lipids. Hyperlipoproteinemia; Fatty Acids, Monounsaturated - administration & dosage; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology; Hypercholesterolemia - drug therapy; Hypercholesterolemia - immunology; Indoles - administration & dosage; Leukotriene C4 - metabolism; Male; Medical sciences; Membrane Fluidity - drug effects; Metabolic diseases; Middle Aged; Neutrophils - cytology; Neutrophils - drug effects; Neutrophils - metabolism; Reactive Oxygen Species - immunology; Reactive Oxygen Species - metabolism; Respiratory Burst - drug effects; Signal Transduction - drug effects; Vasoconstrictor Agents - pharmacology; Human; Peptide hormone; Metabolic diseases; Lipids; Patient; Hyperlipoproteinemia; Lipoprotein; Cholesterol; Octapeptide; Renin angiotensin system; Hypercholesterolemia; Respiratory burst; Neutrophil; Dyslipemia; Angiotensin II
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/j.metabol.2005.03.021

The aim of this study was to investigate the effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor fluvastatin (Flu) on angiotensin II (AII)–stimulated neutrophils of patients with hypercholesterolemia. Results suggest that a 6-week-long Flu administration completely counteracted the AII-induced increase in superoxide anion and leukotriene C 4 production of the neutrophils of patients with hypercholesterolemia. However, the failure of signal processing through pertussis toxin–sensitive G protein, the increase in [Ca 2+] i in membrane-bound protein kinase C activity, and the increase in neutrophil-bound cholesterol content were only partially restored by Flu. In addition, Flu had no effect on the increased membrane rigidity of the neutrophils of patients with hypercholesterolemia. To sum it up, Flu administration had a beneficial effect on AII-triggered reactive oxygen species generation; it resulted in partial restoration of signaling processes and of membrane composition, but membrane fluidity remained unchanged.