11. Chemical Control

• responds to three potential stressors - hypoxia, hypercapnia and acidosis
• carotid body is found at the carotid bifurcation, when stimulated generates action potentials in sensory nerve which feeds into glossopharyngeal nerve to nucleus tractus solitarius in brain stem
• aortic bodies found outside aortic arch, when stimulated transmit action potentials via vagus nerve to nucleus tractus solitarius
• carotid body and aortic bodies are peripheral chemoreceptors, after input into NTS there is medullary integration that modifies central pattern generators that generate inspiratory rhythms

  • modulates diaphragm to change respiration
• the carotid body detects blood hyperoxia

  • hyperbolic response, only see an increase in action potentials when PaO2 is less than 60mmHg
  • increased CO2 makes carotid body more sensitive to hypoxia
• O2 sensory in carotid body detects hypoxia -> closes K+ leak channels -> decreases K+ efflux -> depolarisation -> Ca2+ influx -> NT release -> stimulates AP
• mitochondrial signalling in carotid body to close K+ leak channels due to decreased ATP and increased ROS in hypoxia
• central chemoreceptors respond to hypercapnia

  • increased CO2 in blood -> some converted to H+ and HCO3- -> CO2 that doesn't convert can cross BBB and form H+ in brain -> stimulates central chemoreceptors

  if only H+ increase, cannot cross BBB

  • therefore doesn't respond to metabolic acidosis
• central chemoreceptor transduction mechanism likely involves pH sensitive K+ leak channels

  • H+ causes them to close leading to depolarisation
• hypercapnia response graph in linear (different to hypoxia)

  • at lower O2 the graph is steeper
• apnoeic threshold = decreased PaCO2 where breathing stops

  • seen in hyperoxia and anaesthesia