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Reciprocal Inhibitory Integration and Respiratory Modulation of Arterial Chemoreceptor and Baroreceptor Inputs to Nucleus Tractus Solitarii
Author(s) -
Moraes Davi J.A.,
Da Silva Melina P.,
Machado Benedito H.,
Paton Julian F.R.
Publication year - 2017
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.31.1_supplement.720.5
Subject(s) - baroreceptor , carotid sinus , chemoreceptor , respiratory system , baroreflex , anesthesia , medicine , cardiology , reflex , blood pressure , heart rate , receptor
The cardiovascular and respiratory reflex responses to activation of the arterial chemoreceptors or baroreceptors are dependent on the phase of respiratory cycle. To determine if the respiratory modulation of the chemoreflex and baroreflex occurs within the nucleus tractus solitarii (NTS), whole cell patch clamp recordings of NTS neurons were obtained in in situ preparations from juvenile rats. Thirty non‐respiratory NTS neurons that were depolarized following activation of the carotid body chemoreceptors (by intra‐arterial injection of sodium cyanide) also exhibited excitatory post‐synaptic currents (EPSCs) in response to electrical stimulation of the ipsilateral carotid sinus nerve (CSN; standard deviation of latency: 0.51 ± 0.02). These cells were also tested for the presence of convergent inputs from both the ipsilateral carotid sinus and aortic baroreceptors. Convergent post‐synaptic inhibition from both carotid sinus and aortic baroreceptors was observed in all chemoreceptive NTS neurons tested. CSN evoked EPSCs were averaged separately during different phases of respiratory cycle. Amplitude of carotid sinus‐evoked EPSCs were significant enhanced during expiration relative to inspiration (p<0.05). Additionally, fifty non‐respiratory NTS neurons were depolarized following activation of either ipsilateral carotid (carotid sinus pressure) or aortic baroreceptors (aortic depressor nerve stimulation; standard deviation of latency: 0.2 ± 0.01) and were found to be more sensitive to aortic than carotid sinus activation (p<0.05). Twenty one neurons depolarized only by activation of aortic baroreceptors, while eleven neurons depolarized only by activation of carotid sinus baroreceptors. Convergent post‐synaptic inhibition from arterial chemoreceptors was observed in all tested NTS baroreceptive neurons. Similar to chemoreceptive NTS neurons, amplitude of aortic baroreceptors‐evoked EPSCs were enhanced during expiration relative to inspiration (p<0.05). The results of the present study suggest that: i) there is respiratory modulation of arterial chemoreceptor and baroreceptors inputs by central respiratory drive at this early stage of the reflex arc and; ii) both baroreceptor modulation of arterial chemoreflex, and chemoreceptor modulation of arterial baroreflexes occurs at the level of the NTS. These data reveal a potential mechanism for the baroreflex enhancement observed when peripheral chemoreceptor afferents are denervated. Support or Funding Information FAPESP: SÃO PAULO RESEARCH FOUNDATION BHF: BRITISH HEART FOUNDATION