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Chemosensing by type-1 cells of the carotid body involves a series of events which culminate in the calcium-dependent secretion of neurotransmitter substances which then excite afferent nerves. This response is mediated via membrane depolarisation and voltage-gated calcium entry. Studies utilising isolated cells indicates that the membrane depolarisation in response to hypoxia, and acidosis, appears to be primarily mediated via the inhibition of a background K(+)-current. The pharmacological and biophysical characteristics of these channels suggest that they are probably closely related to the TASK subfamily of tandem-P-domain K(+)-channels. Indeed they show greatest similarity to TASK-1 and -3. In addition to being sensitive to hypoxia and acidosis, the background K(+)-channels of the type-1 cell are also remarkably sensitive to inhibition of mitochondrial energy metabolism. Metabolic poisons are known potent stimulants of the carotid body and cause membrane depolarisation of type-1 cells. In the presence of metabolic inhibitors hypoxic sensitivity is lost suggesting that oxygen sensing may itself be mediated via depression of mitochondrial energy production. Thus these TASK-like background channels play a central role in mediating the chemotransduction of several different stimuli within the type-1 cell. The mechanisms by which metabolic/oxygen sensitivity might be conferred upon these channels are briefly discussed.

Original publication




Journal article


Respir Physiol Neurobiol

Publication Date





55 - 64


Animals, Carotid Body, Chemoreceptor Cells, Humans, Mechanotransduction, Cellular, Mitochondria, Nerve Tissue Proteins, Potassium Channels, Tandem Pore Domain