High PCO does not alter pHi, but raises [Ca2+]i in cultured rat carotid body glomus cells in the absence and presence of CdCl2

We measured the effect of high P CO (500–550 Torr) on the pH i and [Ca 2+ ] i in cultured glomus cells of adult rat carotid body (CB) as a test of the two models currently proposed for the mechanism of CB chemoreception. The metabolic model postulates that the rise in glomus cell [Ca 2+ ] i , the initiating reaction in the signalling pathway leading to chemosensory neural discharge, is due to [Ca 2+ ] release from intracellular Ca 2+ stores. The membrane potential model postulates that the rise in [Ca 2+ ] i comes from influx of extracellular Ca 2+ through voltage-dependent Ca 2+ channels (VDCC) of the L-type. High P CO did not change pH i at PO 2 of 120–135 Torr, showing that CO-induced changes in [Ca 2+ ] i are not due to changes in pH i . High P CO caused a highly significant rise in [Ca 2+ ] i from 90±12 nM to 675±65 nM, both in the absence and in the presence of 200 μM CdCl 2 , a potent blocker of L-type VDCCs. This result is fully consistent with release of Ca 2+ from glomus cell intracellular stores according to metabolic model, but inconsistent with influx of extracellular Ca 2+ through VDCCs according to the membrane potential model.