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Superoxide formation induced by angiotensin II in the rostral ventrolateral medulla is enhanced by high salt diet in rats
Author(s) -
Braga Valdir A
Publication year - 2010
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.24.1_supplement.809.7
Subject(s) - saline , angiotensin ii , superoxide , endocrinology , medicine , chemistry , rostral ventrolateral medulla , hexamethonium , renin–angiotensin system , stimulation , blood pressure , heart rate , enzyme , biochemistry
Here, we investigated the association of dietary salt and angiotensin II (Ang‐II) infusion on hypertension and superoxide formation in the RVLM. Male Wistar rats were subcutaneously implanted with 14‐day osmotic minipumps containing either Ang‐II (150ng/Kg/minute) or saline (0.9% NaCl). In addition, starting at 7 days before drug infusion and continuing throughout the infusion period, rats had free access to drinking water containing 0.4% or 2.0% NaCl. For ROS accumulation measurements in the RVLM, brains were harvested at 15 days of infusion and were submitted to the dihydroethidium technique. Rats that received Ang‐II + water with 0.4% NaCl (G1) became hypertensive after 14 days of Ang‐II infusion (118±5 mmHg vs 98±4 mmHg, n=9, P<0.05). Rats that received Ang‐II + water with 2% NaCl (G2) had a significantly greater hypertension compared to G1 (165±7 mmHg vs 118±5 mmHg, n=10, P<0.05). Rats treated with saline infusion + 2% NaCl‐containing water (G3) or saline infusion + water with 0.4% NaCl (G4) did not become hypertensive (99±3 vs 98±4 mmHg, n=8 and 96±5 mmHg vs 98±4 mmHg, n=7, respectively). Furthermore, administration of hexamethonium (30 mg/Kg i.v.) reduced hypertension in G1 and G2 groups. The magnitude of superoxide formation in the RVLM was G2>G1>G3=G4 (G2= 123±10 Δ %; G1= 67±9 Δ%, P<0.05; and G3=5±3 Δ%, P>0.05), normalized by the G4 group (control). We suggest that dietary salt potentiates Ang‐II‐derived superoxide formation in the RVLM, due to an increase in the inputs within the forebrain‐PVN‐RVLM axis, leading to further increases in sympathetic nerve activity, resulting in a more severe hypertension. Supported by CNPq.