Abstract
Arterial and airway chemoreceptors respond to acute hypoxia by depolarizing, thereby activating voltage-gated Ca 2+ channels and so permitting Ca 2+ entry to trigger transmitter release. Following periods of prolonged hypoxia, these cells undergo a form of remodelling which involves altered expression of ion channels. Here, we use microspectrofluorimetric recordings of voltage-gated Ca 2+ entry (activated by exposure of cells to 50 mM K +) to show that chronic hypoxia suppresses such Ca 2+ entry in model airway chemoreceptor (H146) cells. Furthermore, Ca 2+ entry via L-type channels is suppressed, whilst entry via N-type channels is greatly enhanced. The suppressed response, together with dramatic remodelling of routes available for voltage-gated Ca 2+ entry, is likely to alter significantly the acute O 2 sensing properties of these cells.
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