Mokashi, A; Roy, A; Rozanov, C; Osanai, S; Storey, BT; Lahiri, S

Brain Research [Brain Res.], vol. 803, no. 1-2, pp. 194-197, 24 Aug 1998

We measured the effect of high P sub(CO) (500-550 Torr) on the pH sub(i) and [Ca super(2+)] sub(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 super(2+)] sub(i), the initiating reaction in the signalling pathway leading to chemosensory neural discharge, is due to [Ca super(2+)] release from intracellular Ca super(2+) stores. The membrane potential model postulates that the rise in [Ca super(2+)] sub(i) comes from influx of extracellular Ca super(2+) through voltage-dependent Ca super(2+) channels (VDCC) of the L-type. High P sub(CO) did not change pH sub(i) at PO sub(2) of 120-135 Torr, showing that CO-induced changes in [Ca super(2+)] sub(i) are not due to changes in pH sub(i). High P sub(CO) caused a highly significant rise in [Ca super(2+)] sub(i) from 90 plus or minus 12 nM to 675 plus or minus 65 nM, both in the absence and in the presence of 200 mu M CdCl sub(2), a potent blocker of L-type VDCCs. This result is fully consistent with release of Ca super(2+) from glomus cell intracellular stores according to metabolic model, but inconsistent with influx of extracellular Ca super(2+) through VDCCs according to the membrane potential model.