CO2/HCO3- modulates K+ and Ca2+ currents in glomus cells of the carotid body.

Abstract

Arterial CO2 and O2 are natural stimuli at the carotid body, the primary peripheral chemoreceptor. CO2 acts synergistically with low oxygen (hypoxia) to stimulate carotid body activity and ultimately ventilation. Carotid body glomus cells are believed to be the primary site for chemotransduction. The cellular mechanism(s) of O2 chemoreception by glomus cells are being delineated. Currently it is believed that chemoreception involves depolarization induced by inhibition of K+ channels that are active at the resting membrane potential in glomus cells. Depolarization initiates Ca2+ influx via voltage-gated Ca2+ channels causing an increase in intracellular Ca2+ that leads to neurotransmitter release. On the other hand, relatively little is known about the mechanism of CO2 chemoreception. As a natural stimulus, CO2 could have direct cellular effects or indirect effects by changing pH (another natural stimulus to the carotid body). This complicates investigation of CO2 effects since the effects could depend on the experimental conditions i.e., whether a physiological buffer is used. In fact, a number of studies have found that using bicarbonate-buffered solutions significantly improves the response of the in-vitro carotid body to hypoxia.1-3