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OXIDATIVE STRESS SUPPORTS BLOOD PRESSURE AND SYMPATHETIC ACTIVITY IN RENOVASCULAR HYPERTENSION
Author(s) -
OliveiraSales Elizabeth Barbosa,
Dugaich Adriana Poli,
Abreu Nayda Parisio,
Carillo Bruno Arruda,
Boim Miriam Aparecida,
Bergamaschi Cassia Toledo,
Campos Ruy Ribeiro
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a737-c
Subject(s) - medicine , renovascular hypertension , blood pressure , mean arterial pressure , endocrinology , nitric oxide , brainstem , ascorbic acid , nitric oxide synthase , oxidative stress , heart rate , anesthesia , chemistry , food science
The aim of this study was to evaluate the effects of Ascorbic Acid (Vit C) on mean arterial blood pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) in renovascular hypertensive rats. Moreover, we compared alterations in the mRNA expression of Neuronal Nitric Oxide Sintase (nNOS), Angiotensin receptor (AT‐1) and interleukin 1â (IL‐1â) in the brainstem. Experiments were performed in male Wistar rats (6 weeks after renal surgery ‐ Goldblatt hypertension model ‐ 2K‐1C). Animals were divided in control (C, n= 6) and hypertensive group (GII, n= 6). Vit C was infused (250 mg/kg, IV) over a 6 minutes infusion period and MAP, HR and RSNA were monitored along 60 minutes. The mRNA expression of nNOS, AT‐1 and IL‐1â were analyzed in the brainstem tissue by RT‐PCR technique. Acute infusion of Vit C in 2K‐1C produced a significant decrease in MAP from 157 ± 7 to 120 ± 19 mmHg in the first minute after infusion. No changes in HR were observed. The reduction in MAP was followed by a significant decrease in RSNA (18 ± 6%). The same Vit C infusion in normotensive rats did not produce any changes in MAP, HR and RSNA. The hypertensive animals presented a significant upregulation in nNOS expression in the brainstem (2.3 AU) compared with Control group (1.3 AU). The AT‐1 and IL‐1â expression were reduced in hypertensive rats compared with normotensive rats (GII 0.15 vs C 0.81 and GII 0.12 vs C 1.1; p<0.001) respectively. Our results suggest a possible role of oxidative stress in the etiology of renovascular hypertension. Supported by CAPES, CNPq‐PRONEX