Depletion of p22phox attenuates the exaggerated sympathetic blood pressure response to glutamate and cold stress in stroke-prone spontaneously hypertensive rats, highlighting the role of NADPH oxidase-derived oxidative stress in the rostral ventrolateral medulla.
Oxidative stress modulation in RVLM may influence sympathetic BP control in SHRSP models; hypothesis-generating and should not yet change practice.
Oxidative stress in the rostral ventrolateral medulla (RVLM), a sympathetic center in the brainstem, was implicated in the regulation of sympathetic activity in various hypertensive models including stroke-prone spontaneously hypertensive rats (SHRSP). In this study, we evaluated the role of the NADPH oxidases (NOX) in the blood pressure (BP) regulation in RVLM in SHRSP. The P22PHOX-depleted congenic SHRSP (called SP.MES) was constructed by introducing the mutated p22phox gene of Matsumoto Eosinophilic Shinshu rat. BP response to glutamate (Glu) microinjection into RVLM was compared among SHRSP, SP.MES, SHR and Wistar Kyoto (WKY); the response to Glu microinjection was significantly greater in SHRSP than in SP.MES, SHR and WKY. In addition, tempol, losartan and apocynin microinjection reduced the response to Glu significantly only in SHRSP. The level of oxidative stress, measured in the brainstem using lucigenin and dihydroethidium, was reduced in SP.MES than in SHRSP. BP response to cold stress measured by telemetry system was also blunted in SP.MES when compared with SHRSP. The results suggested that oxidative stress due to the NOX activation in RVLM potentiated BP response to Glu in SHRSP, which might contribute to the exaggerated response to stress in this strain.
No takes yet. Share an insight, caveat, or question.
Zahid et al. (2016) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: