Losartan Reduces the Immediate and Sustained Increases in Muscle Sympathetic Nerve Activity after Hyper-Acute Intermittent Hypoxia.

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxemia (IH), which produces elevations in sympathetic nerve activity (SNA) and associated hypertension in experimental models that persist beyond the initial exposure. We tested the hypotheses that angiotensin receptor blockade in humans using Losartan attenuates the immediate and immediately persistent increases in (a) SNA discharge and (b) mean arterial pressure (MAP) after hyper-acute intermittent hypoxia training (IHT) using a randomized, placebo controlled repeated-measures experimental design. We measured ECG and photoplethysmographic arterial pressure in 9 healthy human subjects, while muscle sympathetic nerve activity (MSNA) was recorded in 7 subjects using microneurography. Subjects were exposed to a series of hypoxic apneas in which they inhaled 2-3 breaths of nitrogen, followed by a 20-second apnea and 40 seconds of room air breathing every minute for 20 minutes. Hyper-acute IHT produced substantial and persistent elevations in MSNA burst frequency (baseline: 15.3 ± 1.8, IHT: 24 ± 1.5, post-IHT 20.0 ± 1.3 bursts/min, all P < 0.01) and MAP (baseline: 89.2 ± 3.3, IHT: 92.62 ± 3.1, post-IHT: 93.83 ± 3.1 mm Hg mm Hg, all P < 0.02). Losartan attenuated the immediate and sustained increases in MSNA (baseline: 17.3 ± 2.5, IHT: 18.6 ± 2.2, post-IHT 20.0 ± 1.3 bursts/min, all P < 0.001) and MAP (baseline: 81.9 ± 2.6, IHT: 81.1 ± 2.8, post-IHT: 81.3 ± 3.0 mm Hg, all P >0.70). This investigation confirms the role of angiotensin II type 1a receptors in the immediate and persistent sympathoexcitatory and pressor responses to IHT.

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