Hypoxia triggers the chemoreceptor cells in the carotid body, leading to increased release of neurotransmitters, particularly catecholamines, which correlates with the severity of hypoxia.
The process involves the depolarization of cells due to the inhibition of oxygen-sensitive K(+) channels, with calcium influx through voltage-operated channels being essential for this response.
Contrary to previous beliefs, maxiK channels do not significantly influence the membrane potential or catecholamine release in rat chemoreceptor cells during both normoxia and hypoxia, suggesting that their complete inhibition is necessary for the cells to spike in response to acute hypoxic conditions.