Renal oxidative stress response to atrial natriuretic peptide in hypertension.

COSTA MARÍA ÁNGELES; ROMERO MARIANA; CANIFFI CAROLINA; BOUCHET GONZALO; MENDES GARRIDO FACUNDO; ELESGARAY ROSANA; TOMAT ANALÍA; ARRANZ CRISTINA

Oslo, Noruega

Congreso; 20th European Meeting on Hypertension; 2010

European Society of Hypertension

Renal oxidative stress response to atrial natriuretic peptide in hypertension. Costa, M.A; Romero, M.; Caniffi, C; Bouchet; Garrido, F.; Elesgaray, R;Tomat, A; Arranz, C. Cátedra de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires. IQUIMEFA-CONICET. mcosta@ffyb.uba.ar   The precise mechanisms leading to the pathogenesis of essential hypertension and renal damage remain unknown. Spontaneously hypertensive rats (SHR) is a model of hypertension which is known to be associates to different risk factors that ends in cardiovascular and renal disease. In previous studies we demonstrated that atrial natriuretic peptide (ANP) infusion increases nitric oxide synthase activity in kidney of SHR, but how ANP can modify oxidative stress in this model of hypertension has not been studied yet. The aim was to investigate the effects of chronic infusion with ANP on renal oxidative stress in SHR. Methods: 8 weeks-old SHR and Wistar Kyoto (WKY normotensive rats) were infused (14 days, subcutaneous osmotic pumps) with ANP (100 ng/hr/rat) or saline (S). After experimental period, we determined in kidney: thiobarbituric acid-reactive substances (TBARS, nmol/mg protein), glutathione concentration (mg/mg protein), and the activity of: glutathione peroxidase (GPx, pmol/min.mg protein), catalase (CAT, pmol/mg protein) and superoxide dismutase (SOD, USOD/mg protein). Results:   TBARS   Glutathione   GPx   CAT   SOD WKY S 0,113±0,015 0,271±0,038 181,1±19,4 0,847±0,102 7,691±0,505 WKY ANP 0,098±0,010 0,398±0,028* 180,3±21,2 0,956±0,098 8,021±1,654 SHR S 0,162±0,025* 0,178±0,046* 243,1±22,1* 0,951±0,105 7,098±0,653 SHR ANP 0,082±0,009# 0,374±0,027# 303,2±30,3# 1,101±0,142 8,452±0,779   *p< 0,01 vs WKY S; #p<0,01 vs SHR S.   SHR shown higher levels of TBARS and GPx activity than WKY rats. Renal glutathione concentration was lower in hypertensive rats than in normotensive ones. CAT and SOD basal activities were similar in both groups and ANP treatment induced no changes their activities. In WKY rats, ANP treatment increased glutathione concentration. In hypertensive rats, ANP chronic infusion diminished TBARS and increased glutathione renal concentration and GPx activity, indicating a reduction in renal oxidative stress. Conclusion: Chronic treatment with ANP improved, almost in part, renal oxidative damage in this model of hypertension in rat.