Key result
Brain angiotensin II receptor blockade and nephrectomy largely prevented acute intermittent hypoxia-induced sympathetic long-term facilitation, which was rescued by central ANG II.
Peripheral RAS activation by acute intermittent hypoxia induces time-dependent neuroplasticity at a central ANG II signaling threshold, triggering a stereotyped sympathetic long-term facilitation response.
May implicate brain angiotensin II in hypoxia-induced sympathetic facilitation; leaves open clinical translation to sleep apnea or related disorders.
Acute intermittent hypoxia (AIH) triggers sympathetic long-term facilitation (sLTF) that relies on peripheral renin-angiotensin system (RAS) activation. Here, increasing AIH cycles from 5 to 10 proportionally increased RAS activity, but not the magnitude of post-AIH sLTF. Brain angiotensin II (ANG II) receptor blockade and nephrectomy each largely prevented sLTF, whereas central ANG II rescued it following nephrectomy. Peripheral RAS activation by AIH induces time-dependent neuroplasticity at an apparent central ANG II signaling threshold, triggering a stereotyped sLTF response.
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Shimoura et al. (2020) studied Acute intermittent hypoxia-induced sympathetic neuroplasticity. Acute intermittent hypoxia (AIH) was evaluated on Sympathetic long-term facilitation (sLTF). Brain angiotensin II receptor blockade and nephrectomy largely prevented acute intermittent hypoxia-induced sympathetic long-term facilitation, which was rescued by central ANG II.
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