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Obstructive Apnea Induces Similar Sympathetic Activation Across Several End Organs Independently of Chemoreceptors Afferents
Author(s) -
Ferreira Caroline B,
Schoorlemmer Gus H.,
Cravo Sergio L,
Stocker Sean D
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.lb722
Subject(s) - splanchnic , medicine , chemoreceptor , apnea , peripheral chemoreceptors , splanchnic nerves , anesthesia , cardiorespiratory fitness , sympathetic nervous system , obstructive sleep apnea , sleep apnea , endocrinology , blood pressure , hemodynamics , stimulation , receptor
Obstructive sleep apnea increases muscle sympathetic nerve activity (SNA) in humans that contributes to cardiovascular dysfunction including hypertension. Several studies suggested that hypoxia is the main mechanism involved in the sympathoexcitation. The purpose of the present study was to determine whether there are regional difference in apnea‐induced sympathetic activation and asses the contribution of carotid chemoreceptors in cardiorespiratory and sympathetic responses induced by apnea. Male Sprague‐Dawley rats (270–350 g) were anesthetized with urethane (1.2 g/kg IV) and prepared for simultaneous recording of renal, splanchnic, and lumbar SNA, phrenic nerve activity (PNA) and arterial blood pressure (ABP). Apneas were performed by clamping a tracheal tube over 20 s while rats were spontaneously breathing room air and repeated in 100%O 2 . Apneas in room air produced similar increases in SNA across several nerves (Δ lumbar: 117±14%; Δ renal: 114±17% and Δ splanchnic: 124±12), hypertension (Δ: 12±2 mmHg), and increased PNA amplitude (Δ: 755±121%) whereas decreased of PNA frequency (Δ: −70±5 burst/m). Hyperoxia reduced the sympathetic activation (Δ lumbar: 56±6%; Δ renal: 40±4%, Δ splanchnic: 47±9%), pressor response (Δ: 6±1) and PNA amplitude (Δ: 570 ± 94%) induced by apnea. In a separate group of rats, to test the contribution of the peripheral chemoreceptor afferents, carotid bodies were bilaterally inactivated. Cardiorespiratory and sympathetic responses by NaCN (0.04%) were abolished but not apnea‐induced responses. Pre‐treatment with ganglionic blockade (chlorisondamine, 5 mg/kg IV) abolished apnea‐induced hypertension (Δ: 2±1mmHg). A last series of experiments were design to assess the effect of neuronal activity blockade and the role of glutamate receptor into NTS. Muscimol or AP5+CNQX cocktail reduced pressor and respiratory responses with no change in sympathetic activation evoked by apnea. Otherwise, importantly reduced cardiorespiratory and sympathetic responses induced by NaCN. Collectively, these findings suggest that other mechanisms rather than hypoxia might contribute for increase in sympathetic outflow induced by obstructive apnea. Support or Funding Information Coordination for the Improvement of Higher Education Personnel (CAPES) and NHLBI R01 HL‐113270, American Heart Association Established Investigator Grant