CuZnSOD Overexpression in the OVLT Does Not Affect Sodium and Water Balance in AngII-Infused Hypertensive Rats.
By utilizing lesion studies, our laboratory has previously demonstrated that both the SFO and OVLT, as well as one of their downstream integration sites, the MnPO, are each independently necessary for the full hypertensive response to elevated AngII [17-22].
In the current study, we report that overexpression of CuZnSOD, an intracellular superoxide scavenging enzyme, in the OVLT significantly attenuates the increase in MAP induced by chronic, peripheral infusion of AngII.
In addition to the SFO, the OVLT is a hypothalamic sensory CVO of significance and part of the originally described anterior ventral 3rd ventricle (AV3V).
in the OVLT as an intracellular signaling mechanism in chronic AngII-induced hypertension.
Downstream of the OVLT, following activation by AngII, the MnPO receives reciprocal inputs from not only the OVLT but also the SFO and is therefore believed to form part of the sympathoexcitatory pathway [10, 11, 33, 34].
While the observations in the MAP response were similar in the present OVLT study to those in the study using overexpression of CuZnSOD in the MnPO , there are some apparent differences.
in the OVLT in mediating the chronic hypertensive effects of AngII.
Caption: Figure 1: Schematic of coronal brain section showing location of OVLT (a).
Caption: Figure 2: Summary data showing average 24-hour mean arterial pressure (a) and heart rate (b) recorded during saline infusion (3 days), AngII infusion (10 ng/kg/min) for 10 days, and recovery saline infusion (3 days) in rats that were OVLT injected with AdCuZnSOD (n = 8) or AdEmpty (n = 6).
Caption: Figure 3: Summary data showing average 24-hour sodium intake (a), sodium output (b), and sodium balance (c) during control saline infusion and subsequent AngII infusion (10 ng/kg/min) for 10 days in rats that were OVLT injected with AdCuZnSOD (" = 8) or AdEmpty (n = 5).