Carotid Body Ablation Reverses the Hypertension and Autonomic Changes Induced by Intermittent Hypoxia

Abstract

Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea syndrome, enhances carotid body (CB) chemosensory discharges in normoxia, eliciting sympathetic overactivation and hypertension. We propose that the enhanced CB chemosensory drive plays a crucial role in the generation of the hypertension during CIH. To study the origin of higher blood pressures during CIH, we performed selective ablation of the CB once animals became hypertensive following CIH exposure. Male Sprague‐Dawley rats (200 g) were exposed to CIH (5% O2, 12 times/h, 8 h/day) and arterial blood pressure (BP) was measured with radiotelemetry. After 3 weeks of CIH, under anesthesia both CBs were cryogenically destroyed with an ice cold needle, and rats were kept one more week in CIH. The effectiveness of this maneuver was confirmed by the disappearance of the ventilatory response to NaCN. After 3 weeks of CIH exposure, rats displayed hypertension (BP~10 mmHg), enhanced hypoxic ventilatory response and reduced baroreflex sensitivity (BRS) from 2.28±0.05 to 1.76±0.10 ms/mmHg. The ablation of the CBs markedly decreases the elevated BP, reduced the enhanced ventilatory response to hypoxia and normalized BRS to 2.52±0.12 ms/mmHg. We found that the cardiorespiratory alterations induced by CIH are critically dependent on functional CB chemoreceptors. Also, our results showed that the CIH‐induced hypertension was abolished by ablation of the CB despite the continuous exposure to CIH stimulation. Thus, our results indicate that the CB plays a pivotal role in the progression and maintenance of the CIH‐induced hypertension.Supported by Puente 28/2014 PUC