Dietary salt enhances angiotensin-II-induced superoxide formation in the rostral ventrolateral medulla

We investigated the association of dietary salt and angiotensin-II infusion on hypertension and superoxide formation in the RVLM. Male Wistar rats were subcutaneously infused with Ang-II (150 ng/kg/min) or saline (0.9% NaCl) for 14 days. In addition, rats had free access to drinking water containing 0.4% or 2.0% NaCl. On the 15th day, rats that received Ang-II + 0.4% NaCl exhibited higher levels of baseline arterial blood pressure than rats that received saline + 0.4% NaCl (118 ± 5 mm Hg vs 98 ± 4 mm Hg, n = 9, P < 0.05). Rats that received Ang-II + 2% NaCl had a significantly greater hypertension compared to Ang-II + 0.4% NaCl (165 ± 7 mm Hg vs 118 ± 5 mm Hg, n = 10, P < 0.05). On the other hand, rats treated with saline + 2% NaCl or saline + 0.4% NaCl did not become hypertensive (96 ± 5 mm Hg, n = 8 and 98 ± 4 mm Hg, n = 7, respectively). Furthermore, administration of hexamethonium (30 mg/kg i.v.) evoked larger decreases in mean arterial pressure in rats treated with Ang-II + 2% NaCl and rats treated with Ang-II + 0.4% NaCl (− 100 ± 5 Δmm Hg and − 72 ± 10 Δmm Hg, P < 0.05). The magnitude of superoxide formation measured by the dihydroethidium technique in the RVLM was greater in the RVLM of rats treated with Ang-II + 2% NaCl (123 ± 10 Δ%, P < 0.05%), than with Ang-II + 0.4% (67 ± 9 Δ%) and saline + 2% NaCl (5 ± 3 Δ%,). The findings indicate that dietary salt potentiates Ang-II-derived superoxide formation in the RVLM, resulting in a more severe hypertension. We suggest that this effect could be mediated by an increase in inputs within the forebrain–PVN–RVLM axis.