Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnoea syndrome (OSA), enhances carotid body (CB) chemosensory activity, produces autonomic dysfunction characterized by higher sympathetic outflow, induces cardiac arrhythmogenesis and promote hypertension. We tested whether autonomic alterations, high prevalence of cardiac arrhythmias and the progression of hypertension induced by CIH are critically dependent on functional CB afferent chemoreflex drive. All experiments were approved by the Bioethical Committee of the Universidad Autónoma de Chile and the P. Universidad Católica de Chile and were performed according to the guidelines of the National Institutes of Health, USA. Adult male Sprague-Dawley rats were exposed to control (sham) conditions for 7 days and then to CIH (5% O2, 12 times/h 8 h/day) for a total of 28 days. At 21 days of CIH exposure, rats underwent bilateral CB ablation (CBA) and then exposed to CIH for 7 additional days. Arterial blood pressure (BP) was measured in conscious rats using radiotelemetry. Additionally, we study the changes in cardiac autonomic imbalance, cardiac baroreflex gain and arrhythmia score during the experiments. Finally, we measured extracellular matrix (ECM) remodelling in cardiac atrial tissue. Compared to Sham rats, CIH rats displayed hypertension (109.8±2.3 vs. 99.9±1.8 mmHg, CIH vs. Sham, respectively, P<.01), heart rate variability shifts towards higher sympathetic tone (Low Freq HRV, 60.6±3.4 n.u. vs. 49.6±3.3 n.u., CIH vs. Sham, respectively, P<.05), reduced baroreflex gain (4.5±0.94 bpm mmHg-1 vs.14.7±1.11 bpm mmHg-1, CIH vs. Sham, respectively, P<.01), increased arrhythmias (184.0±22.4 events/h vs. 101.8±25.7 events/h, CIH vs. Sham respectively, P<.01) and a 1.5 fold increase in atrial collagen content. Remarkably, rats exposed to CIH but that underwent CBA exhibit a marked and significant reduction in BP (pre vs. post CBA, 135.5±2.2 vs.124.2±2.1, P<.01), reduced low freqHRV (pre vs. post CBA, 60.6±3.4 n.u. vs. 43.9±3.5 n.u., P<.05) and reset the midpoint operating point of the cardiac baroreflex (pre vs. post CBA, 111.5±5.6 mmHg vs.102.1±1.65 mmHg, P<.05). In addition, CBA reduced the number of arrhythmias by 60% in CIH rats. Interestingly, CBA failed to restored cardiac ECM remodelling. Our results show that autonomic alterations induced by CIH are critically dependent on the CB and support a main role for the CB in the CIH-induced hypertension. In addition, our results suggest that reductions in arrhythmia incidence during CIH were related to normalization of cardiac autonomic balance and not to cardiac tissue fibrosis.