title: Myocardial oxidative stress and antioxidants in hypertension as a result of nitric oxide synthase inhibition.
abstract: Rats were made hypertensive by the administration of the nitric oxide synthase inhibitor nitro-L-arginine (LNA, 2.74 mmol/L) in drinking water for 7 d. Hearts from hemodynamically assessed animals were analyzed for lipid peroxidation (LPO), gamma-glutamylcysteine-synthetase (gamma-GCS), glutathione disulfide reductase (GR), glutathione peroxidase (GSHPx), catalase (CAT), superoxide dismutase (SOD), and total radical trapping potential (TRAP) activities. LNA treatment increased the mean arterial blood pressure by 46% and the heart rate by 22% without changing plasma renin activity. LNA treatment resulted in a 30% increase in LPO. gamma-GCS was reduced by 48% and GR by 36% in the cardiac tissue of hypertensive rats as compared to controls. The activity of nonselenium GSHPx was reduced by 27%, and selenium-dependent GSHPx activity in the heart was not affected by LNA treatment. In hypertensive rats, SOD activity was increased by 16%, and CAT was decreased by 46%. TRAP was lower (27%) in the myocardium of hypertensive rats than in that of controls. These data suggest that LNA-induced hypertension is associated with increased myocardial oxidative stress.
authors.affiliation: Laboratorio de Fisiologia Cardiovascular, Departamento de Fisiologia, Universidade Federal do Rio Grande do Sul, Porto Alegre, 90050-170-RS, Brazil.
authors.forename: A
authors.initials: A
authors.lastname: Belló-Klein
authors.forename: P M
authors.initials: PM
authors.lastname: Bock
authors.forename: M
authors.initials: M
authors.lastname: Travacio
authors.forename: S M
authors.initials: SM
authors.lastname: Senna
authors.forename: S
authors.initials: S
authors.lastname: Llesuy
authors.forename: P I
authors.initials: PI
authors.lastname: de Bittencourt
authors.forename: M C
authors.initials: MC
authors.lastname: Irigoyen
authors.forename: A A
authors.initials: AA
authors.lastname: Belló
authors.forename: D
authors.initials: D
authors.lastname: Kumar
authors.forename: P K
authors.initials: PK
authors.lastname: Singal
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005721:Glutamate-Cysteine Ligase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced* / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D019335:Nitroarginine / Q000494:pharmacology*; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012083:Renin / Q000097:blood; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D004791:Enzyme Inhibitors; D019335:Nitroarginine; D002374:Catalase; D005979:Glutathione Peroxidase; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D012083:Renin; D005721:Glutamate-Cysteine Ligase; D005978:Glutathione