Carotid chemoreceptor control of muscle sympathetic nerve activity in hypobaric hypoxia

Abstract

High altitude hypoxia causes pronounced sympathoexcitation but the underlying mechanisms remain unclear. We tested the hypothesis that intravenous infusion of dopamine to attenuate carotid chemoreceptor responsiveness would reduce muscle sympathetic nerve activity (MSNA) at high altitude. Nine healthy individuals (mean [SD]; 26 [4] yr) were studied at sea level (SL, Zurich) and at high altitude (ALT, 3454 m, 15–17 days after arrival), both while breathing the ambient air and during an acute incremental hypoxia test (8 × 3 min stages, P_ETO₂ 90-45 mmHg). Intravenous infusion of dopamine (3 μg·kg⁻¹·min⁻¹) and placebo (saline) were administered on both study days, according to a single blind randomized cross-over design. Sojourn to high altitude decreased P_ETO₂ (to ≈60 mmHg) and increased minute ventilation (V_E; mean±SE; saline [SL, ALT], 8.6 ± 0.5 to 11.3 ± 0.6; dopamine, 8.2 ± 0.5 to 10.6 ± 0.8 L·min⁻¹; P < 0.05) and MSNA burst frequency by ≈80% (saline [SL, ALT], 16 ± 3 to 28 ± 4; dopamine, 16 ± 4 to 31 ± 4 bursts·min⁻¹; P < 0.05) when breathing the ambient air, but were not different with dopamine. Increases in MSNA burst frequency and V_E during the acute incremental hypoxia test were greater at ALT than SL (P < 0.05). Dopamine did not affect the magnitude of the MSNA burst frequency response to acute incremental hypoxia at either SL or ALT. However, V_E was lower with dopamine than saline administration throughout the acute incremental hypoxia test at ALT. These data indicate that intravenous infusion of low-dose dopamine to blunt the responsiveness of the carotid chemoreceptors does not significantly decrease MSNA at high altitude.

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