Abstract
Previously, we showed that baroreflex control of heart rate (HR) is reduced but aortic baroreceptor afferent function is enhanced in CIH rats. The goal of this study was to determine the effect of CIH on NTS. F344 rats (4 mo) were exposed to either room air (RA; n=10) or CIH (6 minutes cycles of 21% and 10% O2, 12‐h/day, n=11) for 35‐50 days. Following CIH exposure, rats were anaesthetized with Ket/Ace. Single‐unit extracellular recording was made of NTS barosensitive neurons responding to mean arterial pressure (MAP) changes induced by descending aorta occlusion and measured from the carotid artery. The baseline MAP and HR were similar in RA and CIH. Baseline NTS neuronal firing was 5.6±0.9 spikes/s for RA (n=24) and 6.1±1.0 spikes/s for CIH (n=29). Aortic occlusion‐induced ΔMAP was similar: 26.7±1.0 mmHg (RA) and 26.7±0.8 mmHg (CIH). The time from 5% MAP increase (relative to baseline) to MAP peak was comparable (RA: 5.3±0.6 s, CIH: 5.4±0.3 s). The time from response threshold (30% increase relative to baseline) to NTS neuron peak response was shorter in CIH compared to RA (4.1±0.3 s vs 5.5±0.5s, p<0.05). The time between 5% MAP increase and NTS response threshold was not different between RA and CIH neurons (3.1±0.5s, 3.6±0.5s). Data from the neurons that had short response time (蠄3 s) were used to construct logistic sigmoidal curves (n = 16/group). Based on Gainmax, we identified two groups of neurons. CIH neurons increased NTS response Gainmax [6.4±4.4 (RA) vs 10.54±3.5 (CIH) in grp 1 and 31.9±3.7 (RA) vs 55.5±9.3 (CIH) in grp 2, p<0.05] and range [78.9±11.9 (RA) vs 131.7±21.2(CIH) in grp 1 and 211.2±34.8 (RA) vs 471.6±120.1 (CIH) in grp 2, p<0.05], but did not alter MAP50. Our data suggest that CIH increased output of NTS barosensitive neurons in rats.
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