Abbreviations: hCSP3 = human caspase-3; hPARP- 1 = human Poly(ADP-ribose)polymerase-1; hAPP= human amyloid precursor protein; hBACE-1 =human [beta]-APP cleaving enzyme 1; hADAM-10=hu-man antiamyloidogenic secretase, a Disintegrin and Metalloproteinase 10; hSOD1
= human Cu,Zn superoxide dismutase; hCAT=human catalase; hGR=human glutathione reductase; hGPx = human glutathione peroxidase: hGADPH (or hG3PDH)=human glyceraldehyde 3-phosphate dehydrogenase.
In addition, increased lipid peroxidation [40, 41], increased sensitivity to kainic acid excitotoxicity , and impaired recovery following nerve injury  have been reported in hSOD1 transgenic mice.
Therefore, we need to consider if hSOD1 overexpression in animals can affect the neural components of the baroreflex loop in healthy animals.
hSOD1 overexpression did not alter baseline MAP and HR, and SNP-induced minimums and PE-induced maximums for MAP changes in C57 and SOD1 mice were comparable (Table 1), which allowed us to investigate baroreflex control of HR over a similar range of blood pressure changes (see the following).
Therefore, overexpression of hSOD1 did not significantly change baroreflex-mediated tachycardia and bradycardia.
01), indicating that hSOD1 overexpression resulted in more sensitive responses than the control, thus increasing the aortic baroreceptor depressor nerve function.
hSOD1 Overexpression Did Not Change Basal Blood Pressure and Heart Rate.
In our study, hSOD1 overexpression had no significant effect on MAP, HR, and BRS in healthy mice.
Baroreflex Control of Heart Rate Not Significantly Affected by hSOD1 Overexpression.
As shown in Figure 5, we found that hSOD1 overexpressing mice showed significantly increased aortic baroreceptor activation slope and gain compared to C57 controls.