Inhibition of Superoxide (O 2 − ) in the Paraventricular Nucleus (PVN) Blunts Angiotensin II (Ang II)‐Induced Elevations in Blood Pressure

Circulating Ang II stimulates neural pathways and increases mean arterial pressure (MAP). Moreover, Ang II increases PVN localized O 2 − . Thus, we hypothesized inhibition of O 2 − in the PVN would blunt Ang II‐induced elevations of MAP. Male Sprague Dawley rats were instrumented with venous catheters for delivery of Ang II (30 ng/kg/min, 15ul/min IV, 1 hour) or saline and arterial catheters for MAP measures. Bilateral cannulae in the PVN were used for microinjections of O 2 − scavenger tiron (10 nmol/L, 100 nl/site) or artificial cerebrospinal fluid (aCSF) in conscious rats ten minutes prior to Ang II or saline infusion. To check cannulae placement bicuculline (150 nmol/L, 50 nl/site) was microinjected into the PVN. Pretreatment with tiron significantly blunted Ang II‐induced increases in MAP [Δin MAP; Tiron/Ang II: 30±4 mm Hg vs. aCSF/Ang II: 50±3 mm Hg). Tiron nor aCSF had altered MAP in saline‐infused rats. No changes in heart rate (HR) were observed. Bicuculine induced a significant increase in MAP and HR (Pre‐injection: 83±5 mm Hg, 368±19 bpm vs. Post‐injection: 100±5 mm Hg, 458±13 bpm), indicating PVN placement of cannulae. These data demonstrate that O 2 − in the PVN plays an important physiological role in Ang II‐induced elevations of MAP. In conclusion, elevations in O 2 − in the PVN may contribute to increased excitatory neurotransmitter activity and hypertension.