Airway obstruction produces widespread sympathoexcitation: role of hypoxia, carotid chemoreceptors, and NTS neurotransmission
In this study, we employed this model to test whether the elevation in SNA was mediated by hypoxia, carotid chemoreceptors, or neurotransmission in the nucleus tractus solitarius (NTS). In anesthetized, male Sprague–Dawley rats, airway obstruction (20s) increased phrenic nerve activity (PNA), arterial blood pressure (ABP), and lumbar, renal, and splanchnic SNA. The changes in SNA were similar across all three sympathetic nerves. Inactivation of chemoreceptors by hyperoxia (100% O2) or surgical denervation of carotid chemoreceptors attenuated, but did not eliminate, the changes in SNA and ABP produced by airway obstruction. To interrupt afferent information from carotid chemoreceptor and extracarotid afferents to the hindbrain, airway obstruction was performed before and after NTS microinjection of the GABAA agonist muscimol or a cocktail of NMDA and non‐NMDA antagonists. Inhibition of NTS neurons or blockade of glutamatergic receptors attenuated the increase in lumbar SNA, splanchnic SNA, renal SNA, and PNA. Collectively, these findings suggest that PNA and SNA responses induced by airway obstruction depend, in part, on chemoreceptors afferents and glutamatergic neurotransmission in the NTS.
The manuscript provides evidence that chemoreceptor activation or excitatory neurotransmission in the nucleus of the solitary tract contributes to sympathoexcitation during airway obstruction. The study highlights potential mechanisms that participate in the elevated sympathetic nerv...
Source: Physiological Reports - Category: Physiology Authors: Caroline B. Ferreira, Sergio L. Cravo, Sean D. Stocker Tags: Original Research Source Type: research
More News: Anesthesia | Anesthesiology | Brain | Cardiology | Cardiovascular | Heart | Neurology | Obstructive Sleep Apnea | Physiology | Reflex Sympathetic Dystrophy | Respiratory Medicine | Sleep Apnea | Sleep Disorders | Sleep Medicine | Study