Effects of chronic quercetin treatment on antioxidant defence system and oxidative status of deoxycorticosterone acetate-salt-hypertensive rats.
We investigated the potential of chronic administration of an oral daily dose (10 mg/kg) of the dietary flavonoid quercetin to prevent hypertension and oxidative stress induced by deoxycorticosterone acetate (DOCA)-salt in rats. We have compared its effects to those produced by the well-known anti-hypertensive drug verapamil, administered orally (20 mg/kg/day). Quercetin and verapamil treatments reduced systolic blood pressure of DOCA-salt rats in approximately 67.6 and 63.3% respectively, producing no effect in control animals. Both drugs reduced significantly hepatic and renal hypertrophy induced by DOCA-salt administration, while only quercetin prevented cardiac hypertrophy. Decreased endothelium-dependent relaxation to acetylcholine of aortic rings from DOCA-salt-treated rats was improved by quercetin, but verapamil only enhanced it in the presence of superoxide dismutase (SOD) plus catalase. Increased plasma and heart thiobarbituric acid reactive substances (TBARS) and total glutathione (GSH) levels in liver and heart, decreased liver glutathione peroxidase (GPX) and liver and kidney glutathione transferase (GST) activities were observed in DOCA-salt-treated rats compared to the control animals. The antihypertensive effect of quercetin was accompanied by normalisation of plasma TBARS values, improvement of the antioxidant defences system in heart and liver, restoring total GSH levels in both organs and altered liver GST and GPX activities, and improving kidney GST activity. Verapamil treatment only restored GSH levels in heart, having no effect on other alterations induced by DOCA-salt chronic administration in the antioxidant defences analysed. In conclusion, quercetin shows both antihypertensive and antioxidant properties in this model of mineralocorticoid hypertension, while verapamil exhibits only antihypertensive effects.
Galisteo
Milagros
M
Department of Pharmacology, School of Medicine, University of Granada, Granada, Spain.
García-Saura
Maria Francisca
MF
Jiménez
Rosario
R
Villar
Inmaculada Concepción
IC
Zarzuelo
Antonio
A
Vargas
Félix
F
Duarte
Juan
J
D000284:Administration, Oral; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D006332:Cardiomegaly / Q000517:prevention & control; D002374:Catalase / Q000097:blood; D003900:Desoxycorticosterone / Q000008:administration & dosage; D005978:Glutathione / Q000032:analysis; D005979:Glutathione Peroxidase / Q000032:analysis; D005982:Glutathione Transferase / Q000032:analysis; D006529:Hepatomegaly / Q000517:prevention & control; D006973:Hypertension / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy*; D007668:Kidney / Q000737:chemistry; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000737:chemistry; D008297:Male; D009206:Myocardium / Q000737:chemistry; D010084:Oxidation-Reduction; D011794:Quercetin / Q000008:administration & dosage*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014665:Vasodilator Agents / Q000008:administration & dosage*; D014700:Verapamil / Q000008:administration & dosage*
D017392:Thiobarbituric Acid Reactive Substances; D014665:Vasodilator Agents; D003900:Desoxycorticosterone; D011794:Quercetin; D014700:Verapamil; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D005978:Glutathione