Inhibition of central angiotensin II-induced pressor responses by hydrogen peroxide

• Published in: Neuroscience Vol. 171; no. 2; pp. 524 - 530
• Main Authors: Lauar, M.R, Colombari, D.S.A, De Paula, P.M, Colombari, E, Cardoso, L.M, De Luca, L.A, Menani, J.V
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ltd 01.12.2010; Elsevier
• Subjects: Amitrole - administration & dosage; Amitrole - pharmacology; Angiotensin; Angiotensin II - administration & dosage; Angiotensin II - pharmacology; Angiotensin II - physiology; Animals; arterial pressure; Biological and medical sciences; Blood Pressure - drug effects; Catalase - antagonists & inhibitors; catalase inhibitor; Fundamental and applied biological sciences. Psychology; Heart Rate - drug effects; Hydrogen Peroxide - metabolism; Hydrogen Peroxide - pharmacology; hypertension; Injections, Intravenous; Injections, Intraventricular; Male; Neurology; Rats; Rats, Sprague-Dawley; reactive oxygen species; superoxide dismutase; Vertebrates: nervous system and sense organs; ATZ; HO; HR; ANG II; intravenous; reactive oxygen species; intracerebroventricular; 3-amino-1,2,4-triazole; superoxide anion; O 2; heart rate; AV3V; hydrogen peroxide; mean arterial pressure; SOD; H 2O 2; i.v; anteroventral third ventricle; arterial pressure; catalase inhibitor; hydroxyl radical; superoxide dismutase; angiotensin II; ROS; i.c.v; hypertension; MAP; O2; H2O2; Reactive oxygen species; Hydrogen peroxide; Enzyme; Superoxide dismutase; Renin angiotensin system; Peroxidases; Catalase; Arterial pressure; Hemodynamics; Oxidoreductases; Angiotensin II
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2010.08.048

Abstract Hydrogen peroxide (H2 O2 ), important reactive oxygen species produced endogenously, may have different physiological actions. The superoxide anion (O2·− ) is suggested to be part of the signaling mechanisms activated by angiotensin II (ANG II) and central virus-mediated overexpression of the enzyme superoxide dismutase (that dismutates O2·− to H2 O2 ) reduces pressor and dipsogenic responses to central ANG II. Whether this result might reflect elevation of H2 O2 rather than depletion of O2·− has not been addressed. Here we investigated the effects of H2 O2 injected intracerebroventricularly (i.c.v.) or ATZ (3-amino-1,2,4-triazole, a catalase inhibitor) injected intravenously (i.v.) or i.c.v. on the pressor responses induced by i.c.v. injections of ANG II. Normotensive male Holtzman rats (280–320 g, n =5–13/group) with stainless steel cannulas implanted in the lateral ventricle were used. Prior injection of H2 O2 (5 μmol/1 μl) or ATZ (5 nmol/1 μl) i.c.v. almost abolished the pressor responses induced by ANG II (50 ng/1 μl) also injected i.c.v. (7±3 and 5±3 mm Hg, respectively, vs. control: 19±4 mm Hg). Injection of ATZ (3.6 mmol/kg b.wt.) i.v. also reduced central ANG II-induced pressor responses. Injections of H2 O2 i.c.v. and ATZ i.c.v. or i.v. alone produced no effect on baseline arterial pressure. Central ANG II, H2 O2 or ATZ did not affect heart rate. The results show that central injections of H2 O2 and central or peripheral injections of ATZ reduced the pressor responses induced by i.c.v. ANG II, suggesting that exogenous or endogenous H2 O2 may inhibit central pressor mechanisms activated by ANG II.