Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

One model of oxygen sensing by the carotid body is that hypoxia depolarises type 1 cells leading to voltage-gated calcium entry and the secretion of neurotransmitters which then excite afferent nerves. This paper revues the mechanisms responsible for the membrane depolarisation in response to hypoxia. It concludes that depolarisation is caused not through the inhibition of calcium activated or delayed rectifier K+-channels but through the inhibition of an entirely new type of background K+-channel. This channel lacks sensitivity to the classical K+-channel inhibitors TEA and 4-AP. New evidence does however reveal that background K+-channels in the type 1 cell can be inhibited by Ba2+ and that Ba2+ depolarises isolated type 1 cells. Intriguingly, Ba2+ is the only K+-channel inhibitor thus far reported to stimulate the carotid body. These studies therefore support the hypothesis that depolarisation of the type 1 cell is an integral part of the oxygen sensing pathway in the carotid body.

Original publication




Journal article


Respir Physiol

Publication Date





179 - 187


Animals, Animals, Newborn, Barium, Calcium, Carotid Body, Cell Hypoxia, In Vitro Techniques, Membrane Potentials, Models, Neurological, Oxygen, Potassium, Potassium Channels, Rats, Signal Transduction