General redox environment and carotid body chemoreceptor function.

Area of Science:

• Physiology
• Cellular Biology
• Neuroscience

Background:

• Carotid body (CB) chemoreceptor cells detect hypoxia to trigger hyperventilation, a vital homeostatic response.
• The precise mechanisms of oxygen sensing by chemoreceptor cells are unclear, with reactive oxygen species (ROS) implicated as mediators.
• The cellular redox environment, indicated by glutathione redox potential (E(GSH)), is a potential factor influencing chemoreceptor cell function.

Purpose of the Study:

• To investigate the relationship between the cellular redox environment and the oxygen-sensing activity of carotid body chemoreceptor cells.
• To determine if oxidative stress affects the homeostatic function of the carotid body.

Main Methods:

• Measurement of glutathione levels and calculation of E(GSH) in rat diaphragms exposed to oxidizing agents.
• Assessment of chemoreceptor cell activity in vitro by measuring neurotransmitter release under normoxic and hypoxic conditions.
• Evaluation of carotid body-mediated hypoxic hyperventilation in vivo following treatment with agents that alter E(GSH).

Main Results:

• Variable relationships were observed between E(GSH) and chemoreceptor cell activity.
• Chemoreceptor cell activity demonstrated independence from the general cellular redox potential (E(GSH)).
• Carotid body-mediated hypoxic hyperventilation remained unaltered in animals treated with agents that decreased tissue E(GSH).

Conclusions:

• Carotid body chemoreceptor cell function is largely preserved even under conditions of oxidative stress.
• The homeostatic role of the carotid body in response to hypoxia is robust and not significantly impaired by alterations in the cellular redox environment.