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SOD1 Overexpression Alters Aortic Depressor Nerve Function but Does not Protect Against Impairment of Baroreflex Heart Rate Control in Chronic Intermittent Hypoxia Exposed Mice

Mice overexpressing Cu/Zn Superoxide Dismutase (SOD1) have been used as a model for investigating effects of increased antioxidant activity in pathologies in which reactive oxygen species (ROS) play a role. Our objective in this study is to determine if human SOD1 overexpression can protect against dysfunction of aortic depressor nerve and baroreflex control of heart rate in chronic intermittent hypoxia (CIH) exposed mice. We used the transgenic mouse line C57B6SJL‐Tg (SOD1)2 Gur/J overexpressing human SOD1 and the non‐transgenic C57BL/6J mice (control). Mice (male, 4 months old, n=8‐9/group) were either maintained in room air (RA), or subjected to 6 minutes cycles of 21% and 5.7% O2 during 12‐h light cycles for 40‐50 days (CIH). Mice were anesthetized with isoflurane. Arterial blood pressure (ABP) and heart rate (HR) were measured from the femoral artery. Sodium nitroprusside (SNP) and phenylephrine (PE) were infused sequentially into the femoral vein to decrease and then increase ABP. Aortic depressor nerve activity (ADNA) was recorded. We found that: HR and mean arterial blood pressure (MABP) were similar between groups. Baroreflex control of HR in response to infusion of PE or SNP was not different in SOD1‐RA animals vs. C57‐RA, and it was decreased to a comparable extent in SOD1‐CIH and C57‐CIH. Recordings of ADNA in response to sequential SNP and PE injection‐induced blood pressure ramps revealed a significantly greater baroreceptor gain in SOD1‐RA compared to C57‐RA (p < 0.01), but CIH exposure significantly decreased ADN baroreceptor gain in SOD1‐CIH compared to SOD1‐RA (P<0.01). Our data suggests that SOD1 overexpression alters ADN function, but does not protect against CIH‐induced baroreflex impairment.