The effects of arterial hypertension on cerebral blood flow remain poorly understood. Hemodynamic responses within the somatosensory cortex have been shown to be impaired in the spontaneously hypertensive rat (SHR) model. However, it is unknown whether arterial hypertension affects oxygen homeostasis in vital brainstem areas that control cardiovascular reflexes. In this study, we assessed vagus nerve stimulation-induced changes in local tissue PO2 (Pt O2 ) in the caudal nucleus tractus solitarius (cNTS) of SHRs and normotensive Wistar rats. Pt O2 measurements were performed using a novel application of fast cyclic voltammetry, which allows higher temporal resolution of O2 changes than traditional optical fluorescence techniques. Electrical stimulation of the central-cut end of the vagus nerve (ESVN) caused profound arterial blood pressure decreases along with biphasic Pt O2 changes in the cNTS, characterised by a rapid decrease in Pt O2 ("initial dip") followed by a post-stimulus overshoot above baseline. The initial dip was found to be significantly smaller in SHRs compared to normotensive Wistar rats even after ganglionic blockade. Post-ESVN overshoot was similar in both groups but was reduced in Wistar rats after ganglionic blockade. In conclusion, neural activity-dependent changes in tissue oxygen in brainstem cardiovascular autonomic centres are significantly impaired in animals with arterial hypertension
