Abstract

Visualization of impairment of the cardiac vagal baroreflex, a clinical hallmark of hypertension, has never been materialized. We undertook this task using an experimental model of neurogenic hypertension that employed intracerebroventricular infusion of angiotensin II in male adult C57BL/6 mice. Based on tractographic evaluations using magnetic resonance imaging/diffusion tensor imaging of the medulla oblongata in the brain stem, we found that the connectivity between the nucleus tractus solitarii (NTS), the terminal site of baroreceptor afferents, and the nucleus ambiguus (NA), the origin of the vagus nerve, was disrupted in neurogenic hypertension, concurrent with impairment of the cardiac vagal baroreflex as detected by radiotelemetry. Intriguingly, we found that the disrupted NTS‐NA connectivity was reversible, and was related to oxidative stress induced by augmented levels of NADPH oxidase‐generated superoxide in the NTS. We conclude that depression of the cardiac vagal baroreflex induced by oxidative stress in the NTS in the context of neurogenic hypertension can be manifested in the form of dynamic alterations in the connectivity between the NTS and NA.

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